text:
Confusion about the construction of the rat's mental map
I'm reading the article "A Topological Paradigm for Hippocampal Spatial Map Formation Using Persistent Homology" by Y. Dabaghian, F. Mémoli, L. Frank, G. Carlsson
I try to understand the following graph:

In part a) of the graph, we are seeing a bunch of colored points. These points are in the hippocampus of the rat as opposed to the idea that these points are in the plane on which the rat is moving, and so each point is a place cell of the hippocampus that has fired at some moment in some place of the plane on which the rat is moving. Normally there is a huge number of points in this picture but we chose to put only those who fired, those who did not fire are deleted from the picture of part a). Also, each point (which means each place cell) has one color, and two place cells having the same color designate that the two place cells are considered identical and will be treated as a single place cell in the part b) of the figure.
In part b), we record the time at which each point has fired, with each point being represented by a bar on the time axis and all the bars are identical (same height, and same thickness).
In part c) the picture is in the plane on which the rat is moving as opposed to the idea that the picture of part c) is in the hippocampus of the rat. In part c) we are trying to derive the place fields from part b). Deriving the place fields means here that we are deriving the path that the rat has taken. In particular, place fields are in the plane on which the rat is moving and not in the hippocampus, and each place field in the plane is determined by seeing which place cells in the hippocampus has fired at that area of the plane.
Is my understanding correct? I'm not a specialist but I need to understand each detail of this graph because my work depends on it. My confusion comes from the fact that there are two regions here: the hippocampus of the rat and the plane on which the rat is moving and I need to be sure in which region the picture is.

You have a couple small misunderstandings that I think are making it hard to understand the figure. There is no map of the hippocampus pictured here!
1) Note: this is a schematic figure. These aren't real data, although there are real data that show this pattern. This is meant to be an easy to understand diagram that explains how place cells work.
2) Panel (a) is EXTERNAL SPACE. Essentially it's a "top down" view of a floor that the rat is running around on.
3) Panel (b) shows spike trains for three different cells: theses cells have been arbitrarily color-coded. The hash shows the times that cells 1, 2, or 3 fired spikes. There are just three cells shown in this figure: there aren't any combinations of cells considered one color or multiple cells in one color, just three cells and three colors.
4) Panel (a) is showing how researchers have connected spiking data, like in (b), to the animal's location. The procedure is this:

Start with a blank map of space.
Record from Cell 1. Every time cell 1 fires, mark a blue dot in panel (a) indicating where the animal was when Cell 1 fired.
Record from Cell 2. Every time cell 2 fires, mark a green dot in panel (a).
Record from Cell 3. Every time cell 3 fires, mark a red dot in panel (a).
(the previous steps could be done for many more than 3 cells simultaneously or in sequence; in this example they are just using 3 cells)

5) Panel (c) is in world space, just like in panel (a), and it shows a hypothesized way that the animal could be using the activity of cells 1, 2, and 3 to determine where it is in space. A researcher recording from cells 1, 2, and 3 could also use those recordings to make a guess of where the animal is. If only cell 3 fires within some window of time (an appropriate window is indicated by the outlined ovals in (b) ), and cells 1 and 2 do not, then the best guess is that the animal is in the upper left area that's shaded only red. If all three cells fire, then the best guess is that the animal is in the very center overlapped region of space.
The dashed line shows a hypothetical path the animal might take through it's environment. If the animal took this path, we'd expect to see place cells firing just like they did in panel (b): first only the blue cell, then blue+green, then all three, then red+green, and finally red only.
6) Very importantly: the animal has way way more cells encoding place than just these three. It would be really confusing to plot them all out in discriminable colors like these, but it is this more complex map with thousands of dimensions that gives the animal a good internal representation of its current location.
Hope this helps!

Thank you very much, the only thing that remains ambiguous is panel a). Indeed, cofiring corresponds to two or the three place cells to fire at the same place in the floor, and when this happens we will see three points with three different colors one over the other as if they make the same point but we don't see any occurrence of this in panel a), could it be that   they did that on purpose for simplicity of the picture since a point with three different colors would not be representable in the picture or did they supposed that there is no cofiring in this picture to make drawing simpler?

also why in panel b) the authors replaced the dots by bars, does this have a meaning or just a mere visualization choice ?

Spikes are point processes in time, whereas space is continuous. a) is a representation of spikes in space; b) is a representation of spikes in time. There's no time dimension in (a), except for how time is represented non-continuously as changes in space. If you notice in (b), even at periods of cofiring, the spikes may not be perfectly synchronous. If the animal moves, the points are in different space. Again, these are also schematic data plotted to give you an idea of what's going on; in real data, you could have thousands more points and might make the figure hard to read.


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Difference between spiking and firing
In the article "A Topological Paradigm for Hippocampal Spatial Map
Formation Using Persistent Homology" by Y. Dabaghian, F. Mémoli, L. Frank, G. Carlsson I read some sentences with huge confusion concerning the use of the termss firing and spiking. Do they mean the same thing? It seems to me that when they say a place cell is firing or a place cell is spiking they refer to exactly the same thing. The confusion comes from using both words in the same sentence as in the following sample sentences from the article (emphasis mine):

Indeed, a rat’s path through a small space can later be re-traced with a high degree of accuracy by recording hippocampal spiking activity during its explorations and then
  analyzing the location, size, and firing rates of a mere 40–50
  place fields [...]
To understand what algorithms the brain might use to decode
  hippocampal place cell firing, then, we should rely solely on the
  information provided by place cell spiking activity [...]
It is, in fact, generally assumed that neurons downstream of the hippocampus interpret place cell spiking patterns based on co-firing [...]
It should thus be possible to trace the emergence of topological information as more and more spikes are fired [...]
There are biophysical variables (firing rates, spike amplitude, etc.) [...]

In your quotes, the terms spiking and firing are used as synonyms. Indeed, both terms refer to the same phenomenon of action potential generation and in this context there is no physiological functional difference between spiking and firing.
However, note that in some contexts there may be a difference, namely some authors distinguish between a neuron spiking and bursting; the former referring to a tonic firing mode, the latter to a bursting firing mode (e.g. Ramcharan et al. (2000)).
Reference
- Ramcharan et al., Vis Neurosci (2000); 17(1):55-62

If they are the same how can we explain the second quote:"To understand what algorithms the brain might use to decode hippocampal place cell firing, then, we should rely solely on the information provided by place cell spiking activity." It seems to me that if we replace spiking by firing the sentence has no meaning at all !!

@palio the authors use it as synonyms.

@palio, AliceD is correct. In that particular sentence they mean 'spiking as opposed to external information' such as the "geometry of [...] the environment". The authors could be more clear overall. I haven't read the paper but I spotted at least a couple of logical fallacies.

I agree except for the bit about spiking and bursting; I don't know of anyone who would say a cell that is bursting is not also "spiking."

@BryanKrause agreed, that's why I say explicitly some authors and adding a reference besides.

@AliceD That's partly why I brought it up, though, because that reference does not refer to tonic patterns as "spiking" and burst patterns as "burst firing" - it uses "spike" and "firing" to refer to both in various places. They also talk about "low threshold calcium spikes" but that's a separate phenomenon that can underlie bursting but is not really part of the action potential itself (and is always delineated by specifically referring to calcium spikes/LTS/low threshold calcium spike).

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What are Haplogroups?
What exactly does the term Haplogroup or Haplotype means?
How is it claimed that people belonging to the same haplogroups have common ancestors?

I understand haplogroup as the group of people that share the same given haplotype for a region of the genome.

what is haplotype?

I understand haplogroup as the group of people that share the same given haplotype for a region of the genome.
A haplotype is the readout of the DNA sequence for a part of the genome in one of the two copies that diploid organisms have. If you start reading the DNA sequence for a given point in the genome from one of your copies and someone else's copies, it will coincide up until a point where there is a change. It is more probable to have longer identical haplotypes if the two people that are compared are related. The closest the relation, the longer their haplotypes will be identical. What breaks haplotype identity are recombination events that happen in the germinal line in the previous generation, and mutations that happen both in the germinal line and the soma (the rest of your body) along time.

haplogroup can be an assumed relationship as well - where ethnic groupings may be assumed to have common regions of variants... (e.g. caucasian, east asian, ashkenazi jews, yoruban africans are commonly referenced haplo groups).

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Do all animals exhibit comparable reflex velocity?
First, my exposure to biology is high-school. Should the answer to the question be obvious - please take a moment to laugh, and then point me in the right direction.
A quick google search (or perhaps my search parameters were wrong) didn't give me what I seek.
Animals usually exhibit some form of reflex. What I'm curious about is this -
Do all animals exhibit comparable reflex velocity? Here I use 'reflex velocity' to mean the amount of time elapsed between stimulus, and initiation of the reflex action.

Well, what I think is that as all organisms are exposed to different types of stress or emergency conditions, so the reflex velocities of different species should vary.

Simply stated, the reflex speeds of diverse animal species should not be the same. First, even within an individual, signal conduction speeds actually vary between nerves, on a fairly significant range of about two orders of magnitude. Conduction speeds between species, and likely even between individuals, will differ. Second, not all species possess the same reflexes, which can be, in fact, quite elaborate neural events. To qualify speeds for similar reflexes, one must use closely related species. I did find one article that found the pupillary light reflex in monkeys is essentially similar to that of humans, but this information is not sufficient to speak of the similarities between reflexes in general between the species.

authors: АЛЕКСЕЙ ТРОФИМОВ


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Are human infants inherently frightened by anything?
Naïve question - feel free to shoot it down.
To the best of my knowledge an infant doesn't really 'shrink' from something without first trying it. Even the action of looking at the fierce expression is undertaken without qualm - squalling comes later (if at all!)
Are human infants inherently frightened by anything?

this is more a developmental psychology question.  I have kids and they are quite easily feeling afraid and threatened.  Being left alone without their parents or other close family is very common.

Loud noises are something that infants of any age certainly are not fond of?


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What use a pair of lips?
Pardon my ignorance ... A lip is apparently a very sensitive tactile device - as it at-least serves to warn it's owner they may just be about to consume something that could cause injury. Primates (including humans), dogs, cats, sheep, buffalo, elephants, some fish, octopodes - to name a few, have a lip.
How have lips evolved to be nearly ubiquitous across animals? Why have they evolved into a beak/bill in some birds & fish? What niche/purpose do they fulfill?

"Why have they evolved into a beak". Is this true? I would guess that lips and beaks evolved to perform occasionally similar functions, but from very different structures, and so lips have not evolved into beaks.

Maybe lips are (nearly) ubiquitous in extant mammals because they all inherited lips from a common ancestor.

I think what you are looking for can be found https://en.wikipedia.org/wiki/Lips#Functions_of_the_lips and https://en.wikipedia.org/wiki/Beak#Functions pretty easily.
To summarize, lips:

Mainly useful in mammals
Food intake
Articulation
Tactile organ
Erogenous zone
Facial expressions

Beaks:

Found in birds
Feeding
Defense
Manipulation of objects
Communication
Heat exchange

What is a lip(s)? A set of muscles around an orifice that can close said orifice.
How about a way to close a hole so that not everything can get in but what we want - to eat, breathe, drink?
The fact that they are also sensitive is just needed so that you can more precisely operate them for whatever need you have.


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Are human eyes equally sensitive to AC, and DC lamps?
Definitely anecdotal.
This friend is hypermetropic, and uses reading glasses. He doesn't have major issues facing car headlights, or using a torch (the one with a bulb - not a white LED). Yet place him in front of a TV/Computer screen, and he'll develop an ache in the eye sockets in no time.
I understand an electric torch, an incandescent bulb, a car lamp are all DC types, whereas a TV/Computer screen is fast changing AC.
Are human eyes equally sensitive to light from an AC, and a DC lamp?

Incandescent bulb also can use ac. Tv screens are different case altogether. It is a flickering light.

Depends on the device. Many lamps work on AC. Fans and motors work on AC.
Incandescent lamps work on the principle of electrical heating which both types of current can do. Semiconductor devices generally use DC because direction of the current is important. TV screens are not continuous light; it is a kind of flickering light. In a previous post, this has been discussed with respect to cats and dogs. You may find it useful.

@WYSIWYG: The link to the other post was helpful. ty (+:

I doubt that it's what kind of electricity provides the power -- rather what wavelengths of the light are emitted.

Let's not confuse the type of power of a light emitting device with the type of light it produces.
This question is not about AC or DC current. It is about flicker frequency, light wavelength and their biological effects.
Flicker frequency
The term "ache in the eye sockets" probably refers to asthenopia.
Human eye cannot detect flicker with a frequeny above 75 Hz. But many computer displays have a refresh rate of 60 Hz [1]. Out of focus and  low refresh rate monitors are known to cause eye strain and asthenopia [2], favored by existing hypermetropia (and other vision issues).

Visual discomfort has been related to 1) the presence of flicker; the possibility to regulate, 2) brightness, 3) height; and 4) inclination of monitor. Asthenopia has resulted statistically correlated to the presence of flicker and to the impossibility of regulating height and inclination of monitor for both sexes. The possibility to regulate monitor brightness has not determined a reduction of visual discomfort either in men or in women [3].

Wavelength
Eye sensitivity is different (see spectral sensitivity):
"Cones SMJ2 E" by Vanessaezekowitz at en.wikipedia / Later version uploaded by BenRG. - Based on Dicklyon's PNG version, itself based on data from Stockman, MacLeod & Johnson (1993) Journal of the Optical Society of America A, 10, 2491-2521d http://psy.ucsd.edu/~dmacleod/publications/61StockmanMacLeodJohnson1993.pdf (log E human cone response, via http://www.cvrl.org/database/text/cones/smj2.htm)
Transferred from en.wikipedia to Commons by User:Richard001 using CommonsHelper.. Licensed under CC BY-SA 3.0 via Wikimedia Commons.
Light color and color contrast matter:

The study results showed that both visual acuity and the subjective visual fatigue were significantly affected by the color of light [4].
Images with excessive energy at medium spatial frequencies (Fernandez and Wilkins, 2008 Perception 37 1098-1113), or that have high color contrast and little or no luminance contrast (Wilkins et al, 2008 Perception 37 Supplement, 144-145) appear uncomfortable or aversive and can induce headaches in hypersensitive observers. Such stimuli are uncharacteristic of natural images [...] [5].

Blue light can also reduce melatonin levels and affect sleep and mood (the studies don't have a strong conclusion though):

Melatonin concentrations after exposure to the blue-light goggle experimental condition were significantly reduced compared to the dark control and to the computer monitor only conditions. Although not statistically significant, the mean melatonin concentration after exposure to the computer monitor only was reduced slightly relative to the dark control condition [6].
All light is not equal: blue wavelengths are the most potent portion of the visible electromagnetic spectrum for circadian regulation. [...] evening use of amber lenses to block blue light might affect sleep quality. Mood is also affected by light and sleep; [...] At the end of the study, the amber lens group experienced significant (p < .001) improvement in sleep quality relative to the control group and positive affect (p = .005). Mood also improved significantly relative to controls [7].

References:

Wikipedia contributors, "Flicker fusion threshold," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Flicker_fusion_threshold&oldid=615159751 (accessed July 29, 2014).
Wikipedia contributors, "Asthenopia," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Asthenopia&oldid=617227613 (accessed July 29, 2014).
Rechichi C, Scullica L. [Asthenopia and monitor characteristics]. J Fr Ophtalmol. 1991;13(8-9):456-60. PubMed PMID: 2081858.
Lin CJ, Feng WY, Chao CJ, Tseng FY. Effects of VDT workstation lighting conditions on operator visual workload. Ind Health. 2008 Apr;46(2):105-11. PubMed PMID: 18413962.
Juricevic I, Land L, Wilkins A, Webster MA. Visual discomfort and natural image statistics. Perception. 2010;39(7):884-99. PubMed PMID: 20842966.
Figueiro MG, Wood B, Plitnick B, Rea MS. The impact of light from computer monitors on melatonin levels in college students. Neuro Endocrinol. Lett. 2011;32(2):158-63. PubMed PMID: 21552190.
Burkhart K, Phelps JR. Amber lenses to block blue light and improve sleep: a randomized trial. Chronobiol. Int. 2009 Dec;26(8):1602-12. doi: 10.3109/07420520903523719. PubMed PMID: 20030543.


text:
Why do mosquitoes not collect blood after platelets activate?
This may be anecdotal...
The Indian sub-continent is in the rainy part of summer. It follows the mosquito population goes up.
So when I sliced my palm, I expected the mosquitoes to collect there in force. Yet whilst they continued to go about their business on the forearms, face and elsewhere - the blood flowing out of my palm held no attraction for them. This even after I deliberately stood still for nearly a minute! Perhaps the clotting process/platelets/etc were a repellent.
Why do mosquitoes not collect blood after platelets activate?

I guess mosquitoes rarely have the opportunity to have available fresh blood. Therefore they did not evolve to recognize blood smell but only sweat smell (skin colors and animal shape). In other words, even if they had the physiology to take advantage of your injury, they are just not adapted to recognize it as an opportunity because they did not evolve for this purpose.

I do not know why they wouldn't try, but there may also be a physical reason why they would not: once platelets are activated, a clot might form and block their alimentary tract.

I just went to an interesting talk about malaria and asked the speaker about this. I will try to source and write an answer, but it would seem that mosquitoes can't detect the flowing blood vs the host (as @Rami.b pointed out).  The cut was probably small enough that there was low chance of the mosquitoes landing there vs the rest of your body.  They seem to be attracted to other excretions we produce constantly.

Here's an interesting publication: http://dx.doi.org/10.1016/j.cell.2013.12.044


text:
Is it possible to produce bread using only microorganisms?
I am wondering if it is theoretically possible to produce bread using only microorganisms. If one lists all the chemical components, proteins fermentation time, etc., is it then doable to combine the needed (engineered) microorganisms in one bio-reactor, let them do their thing and produce the wanted product (bread in this case)? Maybe there is a review paper on this topic but I haven't found it yet.
My background: Molecular biology, I know too little about microbiology and bio-reactors, etc.

What do you mean by "only using microorganisms"? Do you mean with no flour at all?

blue green algae and brown algae might be a candidate, it is already used as a minor source for gluten free bread, you would need to specially breed them however to get the right protein to starch levels

@LinuxBlanket Yes, flour provides the structure of the bread. So I can imagine that if an bacteria species is engineered in such a way that it produces every component of flour then it could be possible to produce bread without flour, right?

I would take this question to WorldBuilding. They love the hypothetical 'What if - how can we" type of questions. And shouldn't any Molecular Bio person have a solid understanding of MicroBio and reactors??? At least in my time, ages ago, I received quite some training in that arena during my bachelor's Biochem

It looks like that yeast has been engineered to produce starch.
First of all, the authors had to knock out the genes responsible for the glycogen metabolism pathway (both glycolysis and gluconeogenesis). Then they introduced eight genes known to belong to the amylopectin biosynthetic pathway. The authors succeeded in having starch granules in yeast.
You could start with this yeast strain to produce your bread. You'll probably need to at least dry them in order to reduce them to some sort of flour (probably a hard one, since the yeast would be rich in proteins); otherwise, some means to purify starch grains from yeast should be devised. Then you'd mix them with water and regular baker yeast and maybe you could obtain a bread-like food!


text:
What happens to the brain during meditation?
I've read several experiments on the internet according to which it is possible to reach a psychedelic state without taking any psychedelic drugs like DMT, LSD and other tryptamine derivatives.
It may sound stupid but I was thinking that the brain produces some minimal amounts of a psychedelic drug.
Maybe it is a tryptamine derivative (from the metabolism of the amino acid tryptophan, or from melatonin). I think that there is an undiscovered biological pathway for endogenous psychedelics (I can imagine DMT or 5-MeO-DMT).
What do you think about this? How can the brain go into a psychedelic state without taking any psychedelic drugs?


text:
How could memory work without long-term potentiation?
At the end of his review on the cell biology of synapse formation (2021), Südhoff claims that

there is scant evidence that long-term plasticity per se is
physiologically important for a behaviour.

This lack of evidence - in the form of specific "manipulations of some molecules with multifaceted roles that happen to affect LTP" -, he continues,

has not curtailed speculation that LTP is involved in memory, drug
addiction, and scores of other human brain activities.

I always considered it a dogma that LTP lies at the heart of memory etc. Does Südhoff's view have many other proponents? And how could the standard view ("long-term memory = long-term potentiation") be so strong without evidence? What is it based on, then? Finally: What are alternatives to LTP to underlie memory?

Though he has had a respected career including a Nobel prize, more recently concerns have been raised about his body of work: https://www.science.org/content/article/nobel-winning-neuroscientist-faces-scrutiny-data-discrepancies-papers Personally, I find that paragraph about LTP to be pretty ridiculous, as many papers show influences of LTP on behavior and mechanisms of LTP are some of the most studied in neuroscience.

But how could he be ridicously wrong? He knows more about synapses (and thus LTP?) than almost everyone on earth. And the article was peer-reviewed in a well-reputed journal.

Peer review doesn't mean flawless, it just means some peers were not sufficiently critical of the paper for an editor to reject it. I could easily see peer reviewers not focusing on some throwaway language that isn't central to the paper itself. Südhoff studies synapses, that doesn't mean he studies LTP. I would summarize his argument as "the stuff I study is more important than the stuff they study" - I'd wager that pretty much every scientist thinks this to one extent or another, just like everyone thinks their own children are the best.

I will not comment on the particular author's views and answer the question in the title.
There are five conceivable theories for neural memory (following Hebb (1)):

Memory is sustained by reverberations of neural activity which persist after the stimulus disappears.
Memory takes place through the creation and elimination of synaptic structures, which re-wire the neural circuits.
Memory subsists by adjusting the size of existing synaptic structures, which re-wire the neural circuits.
Memory is internalized by cells through homeostatic adjustments in their molecular machinery.
Memory is simply a re-arrangement of the connections between cells through microscopic movements of the synaptic elements (such as axonal boutons and dendritic spines).

An early proponent of 1 was Lashley. Today, 1 is widely thought largely incompatible with existing evidence, although it can arguably play a role in the formation stage of memory.
Theory 2 consists of the formation and elimination of new synaptic contacts. In most cases studied, i.e. in the cortex and the hippocampus, it appears that this comes down to the formation and elimination of dendritic spines.
Long-term potentiation (LTP) and long-term depression (LTD) come into play with theory 3.
Homeostatic regulation can refer to many different processes, such as changes in synaptic or non-synaptic distribution of some resource such as mRNA or actin, or changes in the distribution and electrical properties of particular types of ion channels and receptors.
Theory 5 is largely incompatible with the apparent mobility allowed in real brains as shown by microscopic evidence.
Theories 2, 3, 4, and 5 are not incompatible with each other. Hebb suggested all four possibilities and only discarded theory 1.
Much earlier, Tanji and Cajal were fighting a similar fight, Tanzi claiming that connections between cells change because the cables change in size (synapses were not discovered yet), while Cajal claiming that new structures must form --later, he changed his mind on this issue.
The association between LTP and memory is overwhelmingly the most popular theory currently in neuroscience and no one could reasonably discard its existence.
However, there is evidence that spine formation and elimination can also play a more limited role in the re-wiring of neural circuits.
It is still an open question to what extent and with what temporal features such re-structuring is coordinated through active processes that could resemble LTP (2), although it is safe to say that activity --thus, likely LTP/LTD-- is involved at some stage (3).
On top of all that, homeostatic plasticity (theory 4) is generally thought to constantly take place, driven by less specific conditions (4).

References
1: Hebb, D. O. (2002). The Organization of Behavior. Routledge. https://doi.org/10.4324/9781410612403
2: Under what conditions do dendritic spines form?
3: Hayashi-Takagi, A., Yagishita, S., Nakamura, M., et al. (2015). Labelling and optical erasure of synaptic memory traces in the motor cortex. Nature, 525(7569), Article 7569. https://doi.org/10.1038/nature15257
4: Do neurons that *don't* fire together unwire?

Nice answer. To connect it back to the paper OP is reading, when Südhoff says "long-term plasticity per se" he means (3); the paper overall is focused on (2). I agree that (2) through (4) are all broadly thought of as critical for understanding long-term memory over time; (1) remains the best model for working/short-term memory though certainly has influences on the others because they are activity-dependent.

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text:
Are all chromosomes equally susceptible to mutation?
The humans have been around for a few million years, other organisms longer yet. Changes that occur in the genome and propagate (may) eventually throw a new species ... or atleast branch off the old one. Are there any chromosomes out there that may be more susceptible to mutation than their neighbours?

Look into recombination hotspots. Also, for reasons of pure statistics, the larger chromosomes are more susceptible to mutation since they have a larger area in which they can accumulate damage.

Are you asking about the mutation rate with or without the effect of selection?

terdon is spot on with the recombination hotspot comment. Mutations are often associated with recombination (information gets lost during crossing-over, so DNA repair is necessary, which of course can introduce mistakes/mutations). It's a fact that there areas in certain chromosomes where recombination happens much more often than other areas of the chromosome. So it follows that chromosomes with more hotspots would likely have higher mutation rates than other chromosomes, on average. This does raise the point, though, that perhaps it's not the mutation rate of the entire chromosome that matters-maybe mutation rates at a more-local level (such as near a hotspot or far away from a hotspot) are more worthy of consideration for your question.
Also, I imagine that sex chromosomes have much lower levels of polymorphism than autosomes. This doesn't have to be because of a lower mutation rate, though: another explanation would be that deleterious recessive mutations on the X chromosome would be purged more easily than on autosomes because their phenotype appears in males (who don't have a second allele because they don't have another X chromosome, so the deleterious phenotype can't be "hidden" like it would in a heterozygote).


text:
Primer Dimer / Hairpin Algorithms
What are the algorithms / methods in use for the calculation of primer dimers and hairpins?
As an example, IDT's OligoAnalyzer tool will generate these analysis given particular sequences.
The homo-dimer analysis seems to me to just be a sliding scan of two sequences across each other. I assume this doesn't take into account possible hairpin issues? or are such structures less likely compared to the myriad of other more common problems.  In addition, how are the ΔG values calculated given a particular dimerization pattern?

It is important visualize more faces to design primer or oligo and PCR experiments:
- calculate thermodynamic parameters of DNA Hybridization (Oligo/Template)

compute hairpin-loop, dimer, bases penality and melting temperature about primer or pair primer
calculate statistics about melting temperature with the change in composition and mix PCR concentration

with google you could find more tools but you must choose a tool of a sequencing team.
almost all tools use mfold algorithm, it's simple and effective:
M. Zuker, D. H. Mathews & D. H. Turner. Algorithms and Thermodynamics for RNA Secondary Structure Prediction: A Practical Guide In A Biochemistry and Biotechnology, 11-43, J. Barciszewski and B. F. C. Clark, eds. , NATO ASI Series, Kluwer Academic Publishers, Dordrecht, NL, 1999.
I worked in a sequencing team and there was a programmer. he developed a fantastic tools. he is a little english, but he could support you: http://promix.cribi.unipd.it/cgi-bin/promix/melting/melting_main.exe


text:
What really happens when a body is tired?
This may be anecdotal; please feel free to vote to close.
After staying awake for an extended duration, I usually find myself having to take extra effort to focus my eyes on an object. Similarly after exerting myself to the extent of near total exhaustion I find it necessary to consciously focus to perform actions that would otherwise require little conscious effort (E.g. Writing a note). There're other similar symptoms almost all of which mandate 'conscious effort'.
What really happens when a body is tired?
As a corollary, why does making conscious effort usually beat the initial error?

Its still not clear why we need to sleep (as distinguished from the question of why our body gets fatigued in physical exertion).  A popular idea is that the brain needs to 'catch up' and reorganize itself given all the stimulus it has had from the previous day.  This 2010 National Geographic article says it all:

I asked William Dement, the retired dean of sleep studies, a co-discoverer of REM sleep, and co-founder of the Stanford Sleep Medicine Center, to tell me what he knew, after 50 years of research, about the reason we sleep. “As far as I know,” he answered, “the only reason we need to sleep that is really, really solid is because we get sleepy.”

It is clear that we need sleep and that we become less reliable at tasks when we are sleep deprived.  eventually we become completely unable to function.
I'm not sure anyone can answer the last question - why does conscious effort help us to perform tasks?  one would have to understand/define the neurology of consciousness to answer that question.  That is still a bigger question that remains open I think.


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Do diurnal birds of prey recognize each other by their appearance?
Just what the title states.
I recognize people around me by their facial appearance to begin with, then by their little idiosyncracies; this applies perhaps to most other humans too. We rely pretty heavily on vision - perhaps because we are a primarily diurnal species gifted with the ability to distinguish colour. But then, so are birds of prey e.g. eagle, kite ...
Do diurnal birds of prey identify each other by their appearance?

Having seen some nature documentaries about Penguins identifying their offspring using sound alone (even in flocks of hundreds of thousands of other birds), my immediate impression was that sound is likely to be more important with regard to recognizing individuals of the same species.
This is corroborated by Melissa Mayntz, a bird enthusiast, who has written a great account on birds use of their 5 senses (Understanding Bird Senses).
To summarize, she explains that whilst sight is a birds most important sense in terms of hunting and avoiding being hunted, their hearing is is their second most important sense and they use this to identify individuals;

Birds hear a smaller frequency range than humans, but they have much more acute sound recognition skills. Birds are especially sensitive to pitch, tone and rhythm changes and use those variations to recognize other individual birds, even in a noisy flock.

Just going to the link (+: Thank you! ... but in the interim I would point out that flocking birds such as the penguin may identify each other differently than loners as birds of prey usually are

@Everyone that is true of course - but I imagine that a bird of prey would call to identify themselves to another bird, as you would have to be much closer to identify by sight. We use sound to identify people easily too - over the phone for example we can easily recognize a voice we know, without having any prior knowledge as to who it may be. I'm speculating of course, but it seems to me that sound would be much more useful to a bird in flight, or in a tree, because you may not be able to see one another!

Recent research has indicated that wild American crows (Corvus brachyrhynchos) can recognize individual human faces (Mazluff et al. 2010).  If crows can recognize individual people, then it might not be too farfetched that other bird groups can recognize each other by appearance.


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What causes instinctive behaviour?
Some actions, almost behaviour, exist that are common across a species. For instance, based on personal observation, human babies try to taste anything new they encounter until they are a few score months old. Similarly most dogs will go round-and-round before they finally settle down to sleep.
We probably use the term 'instinctive' to indicate there is no conscious thought behind that action, albeit the action is not a reflex either. Anyway, what causes instinctive behaviour? Is it genetic in nature? Are there some basic rules/behaviour hard-coded into our brains sort of like BIOS in a computer?

If it's present across an entire species through multiple generations, then it implies that the behavior is inherited - so yes, genetics would play a role. If genetics play a role, then the behaviors are "hard-coded" into our physiology.

I just want to point out that behaviour is often divided into instinctive (including reflexes) and learned. Behaviour can be learned even if the species is not conscious, and repetetive behaviour can be learned. Remember that few species are conscious (maybe none, depending on your definition), so consciousness is not necessarily useful to discuss general instinctive behaviour.

This stuff is so interesting! The instinctive behaviour is also known as a fixed action pattern or FAP which is a collection of well-defined motor patterns that are activated in response to a stimulus, i.e. a group more eleborate reflexes [2]. FAPs allow the brain to concentrate on other things as they don't need require time or energy to be thought about. The theory is they've been selected for because they decrease choice and decision time, which can be particularly important to survival.
There are some cool examples here (http://www.cerebromente.org.br/n09/fastfacts/comportold_i.htm).

the bird is continues to perform parental instinctive behaviour in the absence of a brood of chicks because the similar stimulus of hungry open-mouthed fish is present.
Another article draws comparisons between different animals as to how much of their behaviour is fixed/pre-determined [3]. There can be a correlation between the size of the cerebral cortex, used for thinking and problem solving, and the amount of innate behaviour (i.e. the bigger your cortex the less you need to rely on pre-determined behaviours in certain situations).
These patterns seem to be for the most part genetically determined, however some studies with song-birds in the 70's demonstrated that a learning aspect can modify the innate behviour. Birds which have been reared in an environemnt where they cannot hear other birds of the same species sing still sing their typical song, but when allowed to hear others sing the song becomes more complex.
Investigating the genetic basis behind innate behaviours involve searching for Quantitative Trait Loci (QTLs) or stretches of DNA that contain genes (complex traits require the concerted actions of multiple genes) or are linked to genes that are involved in determining a specifc trait (in this case a behaviour). Classically this involves crossing two animals that differ in the trait you're interested in and looking at the segregation patterns in the offspring to try and pinpoint the specifc region of DNA/collection of genes that control the trait. I think quite a lot of this has been done in insects and mice which have high breeding rates and can be studied easily in the lab.
...at this risk of making this answer ridiculously long I've just included a snippet from another website on behavioural genetics which details the OMIM and some of the traits you can search for[4]:

Online Mendelian Inheritance in Man (OMIM) is a large, searchable, up-to-date database of human genes, genetic traits, and disorders. Each OMIM record contains bibliographic references and a summary of the scientific literature describing what is known about a particular gene, trait, or disorder. The following behavioral traits are included in OMIM. The six-digit number MIM number is used to uniquely identify each record.

Hand skill, relative (handedness): (139900)
Hand clasping pattern: (139800)
Arm folding preference: (107850)
Ears, ability to move: (129100)
Tongue curling, folding, or rolling: (189300)
Musical perfect pitch: (159300)

[2] http://books.google.co.uk/books?id=aQvGXLPjMPAC&pg=PA44&lpg=PA44&dq=fixed+action+patterns+difference+reflex&source=bl&ots=TxaSYeIpTs&sig=RfsmHLWVlNiF8B-dH928-F0I5M8&hl=en&sa=X&ei=Bs1WUZeCFYiZtAbZ_IHYBw&ved=0CDcQ6AEwAA#v=onepage&q=fixed%20action%20patterns%20difference%20reflex&f=false
[3] http://www.grandin.com/references/genetics.html
[4] http://www.ornl.gov/sci/techresources/Human_Genome/elsi/behavior.shtml


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What causes the characteristic 'gleam' in the eye of a living being?
The title is pretty much what I seek to know.
Unless the other person is play-acting, one can often make out the eye of a living person has a shine-of-life to it; a cadaver does not. Similarly the gleam appears brighter when a person is feverish, or excited otherwise ... or has some infection in the eye itself.
What causes this gleam? Is it merely nervous electricity at work that disappears when the system is shutdown/crashed?

I think this is good question. The mysterious part is that sexy, energetic people seem to have special "gleam", while those lacking enegy do not have. Is it hormonal-related ? I am pretty sure nobody did research on this.

@Andrei, can you back that up with evidence? I've never ever heard that before...

Not being an opthalmologist, if one happens along and gives a better/correct answer, listen to them.
Otherwise, let's take a moment to look at the eye:

What is not pictured here is the saline-like solution that keeps the conjuctiva moist. If we include the lubrication in all of the surfaces which interact with light, our list would look like this:

Lubrication
Conjuctiva
Cornea
Anterior aqueous humour
Iris
Posterior aqueous humour
Lens
Vitreous humour
Retina
Fovea

Out of that list, the Iris, Retina, and Fovea are designed to absorb light; not reflect it. The Vitreous humour merely serves as a medium for light to pass through and probably would not reflect light on its own. The same is true of both aqueous humours - they do not modify the light so much as serve the eye structurally.
That leaves us with the Lubrication, Conjuctiva, Cornea, and Lens - surfaces which also interact with light, but act to some extent to reflect or modify it as well. The Cornea is what's actually operated on when a person undergoes corrective surgery; a pattern is etched into the Cornea which redirects light similar to the person's previous prescription and giving them better vision.
Now, because you mention the difference between an excited person and presumably someone at their normal state, it's worth to note (when dealing specifically with the eye) a very common side-effect of psycho-active drugs and emotional states (particularly fear and interest/curiosity) is the change in pupil size when lighting conditions don't change:

The reflection is different depending on the size of the pupil, and I would venture to guess the pupil size difference between someone who's excited or manic (whose system is flooded with endorphins) and the person at normality is part of what you define as 'gleam.'
The other situation you draw a difference between is a dead person vs. a living person. Before rigor mortis sets in, the relaxed state of the ciliary body is to stress the suspensory ligaments - resulting in pupil dilation. In addition, and I think this is the most important distinction: dead people don't blink. The act of blinking spreads the lubrication on the surface of the conjuctiva, and can be mimicked with tear-drops for people with dry eyes. Because the lubrication acts as another surface to reflect light (similar to having a thin layer of water on a surface), the dead person's eyes will have less of a "gleam" than a living person's.
So, to sum up: The "gleam" in a person's eye is probably due to hydration and/or pupil dilation. Pupils will dilate at lower light levels, under the influence of certain drugs, or when showing interest. Hydration is constant, except when the lubrication is not produced in the quantities necessary or when the person is unable to blink ('dead' in your example).

Also worth noting that circulation stops at death, causing changes to the appearance of the eye over time.  See e.g. http://www.defrostingcoldcases.com/guest-post-post-mortem-ocular-changes-are-not-conclusive-post-mortem-interval-evidence/


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Are intracortical axon branches myelinated?
I found the following pictures of axon trees:

source

source (axons are red)
but didn't find a concise answer to the following question:

Is it possibly true that the intracortical axon branches (i.e. those that don't leave the gray matter) are not
  myelinated?  (The first picture seems to indicate that they have at
  least a smaller diameter, making them slower?)

A great reference for this question is Tomassy et al. 2014. Axons of cells from all layers lack a myelin sheath at their proximal segment, often called the axon initial segment. This stretch of unmyelinated axon is longer for more superficial pyramidal neurons (~150 $\mu m$) and shorter for those located in deeper layers (~25 $\mu m$), something which does not depend on axonal caliber. These authors observed that some of the superficial neurons didn't have any myelin for the length of axon observed (> 200 $\mu m$). They speculated that these are neurons that send their axons through the corpus callosum.
What is interesting is that superficial pyramidal neurons often displayed intermittent myelination away from that initial segment, with long stretches of axons (up to ~55 $\mu m$) being unmyelinated. Note that these myelin gaps are more than an order of magnitude longer than Ranvier's nodes.
What are these gaps in myelin good for? If these axons target other intracortical neurons, it is unlikely that the predicted transmission delay will have an important impact given the short distances in the cortex (~1 mm). For those neurons targeting other brain areas it may be somewhat more important. It is interesting, however, that these patches of unmyelinated axons both made and received synapses, suggesting that they may have a functional role.
The neurons in the OP's images are corticothalamic cells residing in (lower) layer 2/3 of the visual cortex (upper half) and thalamorecipient cells in layer 4 of the motor cortex (bottom half). Thus it is likely that their axon initial segment is unmyelinated. Although not yet conclusive, the results of the cited paper support the view that the axons of those superficial neurons that project to deeper layers or other brain areas are completely unmyelinated.

modified from wikipedia, CC BY-SA 3.0


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How to mark an ant with the least disturbance to the ant and the nest
How would one go about marking one or more ants in a nest so as to least disturb the ant and the nest? The goal is to be able to know which ant you marked months, or many years up to a lifespan later, while at the same time have the least influence of the markings on the behavior of the ant and the interaction between the marked and not-marked ants.

lots of previous research has been done marking bees and ants.

For this purpose, people usually paint ants on top of the thorax (not on the head where it can prevent eyes and antenna to function normally, nor on the abdomen where it can block the spiracles and prevent respiration), with a bit of acrylic paint applied with a toothpick. Combination of colors are used to identify individuals.
These techniques are currently being replaced by the use of RFID tags and Flashcodes in science, to automate recordings.


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Effect and functional role of voltage-gated channels on dendrites
I'd like to understand better the effect and functional role of voltage-gated channels on dendrites.
What I believe to have understood:

It is important that a more distal post-synaptical potential (PSP) arrives at roughly the same time and with roughly the same strength at the soma than a more proximal PSP generated at the same time (to give them comparable weights and to detect that they were synchronous). Let me call this the goal of adjustment.
Achieving this goal is the main function of (properly distributed) voltage-independent channels on dendrites (→ Rall model)
The main function of voltage-gated channels on axons is unattenuated signal transport.
Voltage-gated channels on the dendrite lead to non-linearities.

The immediate physical effect of voltage-gated channels on the dendrite is hard for me to imagine and understand. But even harder to understand are the (specific) functional advantages and disadvantages of those channels.
Some possibilities come to mind:

They allow to achieve adjustment better (more precisely) or in some other way more efficiently.
They allow to achieve other goals better or more efficiently (which are only poorly achieved without them).
They allow to achieve completely new goals which are not achievable at all without them (by having some magic computational powers due to non-linearities).
They may have disadvantages (which should not exceed there advantages, otherwise they would not exist), e.g. by distorting PSPs in an unwanted way.

I know that there is a lot of literature on the topic of dendritic processing, but not so many gentle introductions. A gentle introduction - answering some of the following question  - would be welcome. And of course immediate answers!

Do voltage-gated channels on dendrites (distributed as they are) allow to achieve adjustment better or in some other way more efficiently?
Which other goals do they allow to achieve better or more efficiently?
Which new goals do they allow to achieve?
Can their extra computational powers be pinned down?
Which disadvantages do they have (possibly)?

[I believe it wouldn't make sense to split this question into five: they are too strongly related, aren't they?]

As on axons, one immediate effect of voltage-gated channels on dendrites is the generation of spikes (called dendritic spikes as opposed to action potentials). These typically have higher local voltage thresholds than on axons. They seem to play a major role in long-term potentation. But it's not obvious for me how, and which other "implications in neuronal communication, memory, and learning" they might have.

Did you read the review I've suggested to you elsewhere? It is reasonably recent and well-written by two of the authorities in the field. Otherwise, I may be able to conjure a thorough answer when I find the time.

This is also very relevant and written in an accessible way (although behind a paywall).

Sorry, I did not  because it is not free and I don't have access.

Same for both references.

https://www.janelia.org/sites/default/files/Labs/Spruston%20Lab/Stuart_Spruston_2015.pdf
https://pdfs.semanticscholar.org/4890/d678183a2e14a65e5669fc929fe8ddb21a10.pdf
PS: I used google scholar to find PDFs in personal archives

@ykehayas: I finally read the papers (at least substantial parts of them) and found a lot of information I was looking for. Thank you for these great references (which I still have to digest, of course).

I look forward to you supplementing your answer based on your research!

I'll better ask better questions.

Is this one better: https://biology.stackexchange.com/questions/66050/simple-model-of-dendritic-processing?


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Identification of a Lepidopteran
I’m afraid the quality of the television picture below isn’t very good, but can anyone identify this moth? It was one of those that invaded the pitch at the Euro Final in Paris on 10th July 2016.

Let me know if my edits translate accurately, to your intentioned meanings

@hello_there_andy — No. Your English was — and is — deficient (intentioned meaning, indeed) and the general edit was poor. If the chatty style offended you and you felt it needed formal time and place I have dealt with this. I commend the revised question to you as an example of succinctness. If you have any further criticism please raise it and I will deal with it or not, but please do not vandalize my English. I am an Oxford educated native speaker.

Noted. And apologies. I enjoy the fact you changed it since :) OP. I will also respect your request to not edit your future work. But believe me, there are certain controls in place to ensure it is not entirely your property. Try deleting some of your answers, to play an example.

@hello_there_andy — I appreciate that questions and answers can be edited by others and understand that they are for the community as a whole. However as I spend considerable time correcting and improving questions from non-native or naive posters, I found your treatment of my question extremely irksome and that of whoever approved the change quite reprehensible.

I really do apologise. I also realise my English might need better practice. You helped me take proactive action to improve it (no sarcasm), TQ.

I didn't watch the game, but from what I've seen on the internet it was the Silver Y (Autographa gamma), drawn there by the lights while migrating http://theconversation.com/moths-expert-match-report-on-ronaldo-insect-encounter-at-euro-2016-final-62314

I couldn't really be completely sure by this picture alone so I did some searching around and turns out it is a Autographa Gamma(Silver Y)

oh, you beat me to it by a second or something!

There is always place for more! Oh and by the way I didn't watch the game either. Was there some kind of "havoc" happening?

i really don't know, all i saw of it was the moth discussions trickling down into my usually sports-free circles.

@Ria — I wouldn't call it havok, but every time the play stopped and the camera zoomed in on a player there seemed to be at least one moth flying round him. And, of course, there was Ronaldo on the ground, in pain, in tears, waiting to be stretchered off, completely oblivious to the moth on his face — unlike the millions watching.

@picapica, actually Ria beat you to it by two mins :) - though, I'm not entirely sure why yours still "won"


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Will neurons die if they are inactive for a long time?
We know that when muscles are not used they atrophy. Does something similar also happen in neurons if they do not receive any stimulus?

Short answer
Yes.
Background
Postsynaptic neuronal degeneration after deafferentation are notorious in the peripheral sensory systems. There, marked degenerative processes are present when input to the secondary neurons is lost due to degeneration of the primary sensory neurons. In other words

When the hair cells are lost in the cochlea, the auditory nerve degenerates (e.g., Kuyama, 2010);
When the retinal photoreceptors are lost, for example due to degenerative diseases like retinitis pigmentosa, bipolar and horizontal cells in the retina degenerate due to a loss of efferent input (Mazzoni et al., 2008). For more information see the works of Marc & Jones, e.g.., Jones & Marc (2005).

Note that in the central nervous system these effects play less of a role, as neurons have ample opportunity to reconnect to other neurons, for the better or worse; e.g., in the hearing impaired and visually impaired, spontaneous sensations of sound and visuals may develop and lead to tinnitus and photopsias, respectively. These symptoms are caused by cortical sensory neurons desperately and randomly looking for sensory input after being deafferented due to peripheral loss of hearing or vision. When they cannot obtain useful input any longer, they gather irrelevant, non-useful input and start generating spontaneous 'illusionary' perceptions instead.
References
- Jones & Marc, Exp Eye Res (2005); 81(2): 123-37
- Kuyama, J Neurosci (2009); 29(45): 14077–085)
- Mazzoni et al., J Neurosci (2008); 28(52): 14282–92

These examples are related to structural loss of contacts, with the retina case occurring in a background of general degeneration. Is the loss of B and H cells due to lack of input or simply the surrounding inflammatory environment? IMO, the OP is asking about loss of inputs or absent activity in otherwise healthy neurons with contacts intact, which is a subtly different question, no? In a non-diseased context, do neurons actually die if they don't fire for a while? Consider long term memories stored in synapses which may not be activated for many years. just my 2 cents..

@LouisLeung there are no inflammatory responses afaik in the cochlea in the case of age related hearing loss and other forms of sensorineural HL so your comment doesn't apply there. In the retina I would have to double check.


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Why do reptiles still move even after death?
I saw a video in which a decapitated snake head still tried to bite.
I also saw a video in which a man was hit by the moving tail of a dead crocodile.
So why do reptiles move even after death?
http://en.wikipedia.org/wiki/Reptile

I think it is not only reptiles - chicken are notorious for dong this, and insects as well: http://biology.stackexchange.com/questions/23842/why-does-a-cockroach-not-die-even-after-decapitation?s=1|1.0349

Perhaps the problem here is with your definition of death?  Death is not (usually) an instantaneous state change, but a gradual process. The decapitated snake or chicken is dying, but not yet dead.

In warm-blooded animals, our high metabolisms are a significant disadvantage when being decapitated. Just a few minutes without oxygen and a mammal's brain is caput—the result of a massive cascading cellular die-off. Not so with cold-blooded reptiles. Their slow metabolism sustains their internal organs for far longer than a mammals causing them to completely die far more slowly. Essentially, cutting off their heads only makes them "mostly dead".

Can you add some references to your answer?

Reptiles stimulate impulses after death due to reasons, lets see snake for example.
Snake after been crushed still moves because of the electrically charged ion in the nerve calls of snake, as the brain continuously send messages through the nerve cells, note that the brain of snake need the least amount of oxygen for survival so does not die as quick as you may think, the brain can still live for about 1hr after the body of the snake stopped stimulating impulses.
Be advised, never put your finger in a Dead snake's mouth as it can still harm.

Welcome to the forum. It's good practice to provide reference for your claims (such as books or scientific publication or at least web pages).


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Why do people eat meat?
My main question is why do people eat meat?
Can we not survive without meat?
I recently became a vegetarian and I have not yet felt any impact on my health. Can any one explain this phenomenon from the perspective of nutrition?

You might note that the health problems caused by dietary deficiencies may take months, years, or even decades to show obvious symptoms.

What do you mean by "spiritual benefits"?

There are many reasons for why people eat meat. Some of them are to be discussed here and some of them have nothing to do with biology.
Reasons that have nothing to do with biology
There are many reasons that are not to be discussed on Biology.SE. These include cultural reasons, the reasons related to taste and appreciation, farming and availability, price and economy and of course for reason related to political ecology (incl. water and energy consumption of meat production).
Reasons that has to do with biology / medicine
We can talk about nutritional value though. According to a number of websites (sorry nothing peer reviewed; monitor.co.uk; rd.com; sparkpeople.com), people not eating meat may suffer from lack of

protein
iron
zinc
calcium
vitamin D
vitamin B12
omega–3 fatty acids

It is not impossible to get all of these nutrients without meats. However, when becoming vegetarian, some people need to be careful and rethink their diet to ensure not to suffer from the lack of these nutrients.

Where do these six come from? Can you support this with a source?

I don't think calcium and vitamin D deficiency are common in vegetarians.

@Remi b - can you highlight the vegan product to get vitamin B12

@Lasantha You can just google it. Amandmilk, coconutmilk and soymilk contain a lot of vitamin B12.

Tribal peoples throughout the world have revered meat since the times of cave paintings, over 30,000 years ago and the oldest stone arrowheads are 66,000 years old.
Chimpanzees also eat meat. They can hunt like wolves and devour small prey. (see videos)
Meat is a highly useful or essential nutrient source to those who cannot source enough local protein for the level of activity.
The importance of meat depends on geographical factors. Eskimos live in snow and eat more than 90% meat. There are no plants there. Equatorial people like Indians have plentiful plant growth and can live fine as vegetarians on replenishing foods like lentils and greens.
Northern people have less choice of vegetables and fruits, whereas tropical fruits like melons grow year round, and northern plants grow slowly, whereas northern grazers can grow fast.
Energy budget in the north is limited by the sun, which is deficient to grow grains and oils. Fat is the highest energy source, and it is very easily sourced from livestock.

Just a minor quibble - India is tropical.

@Roni Saiba: Depends on what part of India you're looking at.  It's a big place, with lots of climate variation, especially when you take elevation into account  :-)

Disclaimer: I am not an anthropologist, this attempt at an answer is only my crude 2 cents, I haven't looked for references to support this supposition.
Nowadays we can survive without meat, but this has not always been so. We know that early human groups were hunter-gatherers. Hunting is obviously much more difficult than gathering: it takes more energy because you have to run, it is more dangerous because you can be hurt in the process. Therefore, the primary reason why early humans hunted and ate meat must be because they had no choice; likely because they could not gather fruits and plants in enough amounts or variety to support a healthy diet. Later on, when they transitioned to agriculture they also naturally transitioned to raising domesticated animals for meat production because that's what their diet was already like.

WRT hunter-gatherers, I don't think it is really because they can't gather enough plant foods, it's that meat offers more food for less effort.  You don't have to run to hunt (unless you want to): you lie in ambush, set snares or pit traps, drive the mammoths over a cliff, &c.  Likewise with subsistence farming: once domesticated, animals like cows, pigs, chickens and such can turn things that really aren't edible by humans (like grass, acorns, small bugs...) into tasty food, with much less effort than is required by plowing, planting, & harvesting crops.


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Dopamine involvement in pleasure
There are some psychologists who believe that dopamine is not released during pleasurable activities but before them; my understanding is that a little dopamine is released pre-reward in order to motivate us to complete the action and then a large amount is released when we consume/get the reward. Can you please explain this? Their argument is that dopamine release tells the brain that it is about to feel good and then the brain releases opioids to make us feel good. This doesn't make sense if when addicts take opioids, such as heroin, the brain is flooded with dopamine and the person feels good. In that case we could say that dopamine is responsible for the euphoria. Do you believe this to be correct?

This is an ongoing discussion, and entire textbooks are written in this field, but I will try to clear up some misconceptions and point you toward some further reading that may help.
Is dopamine pleasure?
"Pleasure" is an emotional phenomenon; dopamine is a neurotransmitter. Dopamine can be involved in the perception of pleasure, but there was a now-outdated hypothesis that "dopamine==pleasure".
More recent evidence says that this is not the case, because endogenous dopamine release occurs in some brain regions during the anticipation of a pleasurable event, and really doesn't correlate with pleasure itself at all. Instead, dopamine is currently thought to reflect a "reward prediction error": a signal that tells the brain "hey, we just got something better than we expected!"
Why is a prediction error useful?
This signal can then be used by the brain to upregulate circuits that were recently active, effectively using the heuristic: "I just got something I didn't expect, so whatever I did just before must have been a better thing to do than I previously thought! I should do that more often!"
There are 'degrees' of unexpectedness, however, which is why you get a dopamine signal when a positive event is expected. Let's say a cue, like a bell, signals a coming reward. The reward is now expected, so it won't produce an error signal, but the bell itself produces an error signal: prior to the bell, you didn't know the bell was coming, so you didn't know the reward was coming. Now you update your brain circuits to try to do things to make bells ring!
This is a powerful learning algorithm that is also used, in a form, in artificial neural networks.
Context in drug abuse
If a drug of abuse causes a release of dopamine, that's a signal to the rest of the brain "Hey, something good just happened, let's try to do that again in the future!" Dopamine is the message, not the experience.
Further reading
The two bolded works below are a recent review and a highly relevant original paper, respectively.
Peter Dayan, Wolfram Schultz, and Ray Dolan were recently awarded for their work in this field and you can find lots of popular press that describes their work, as well.

References
Schultz, W. (2013). Updating dopamine reward signals. Current opinion in neurobiology, 23(2), 229-238.
Schultz, W., Dayan, P., & Montague, P. R. (1997). A neural substrate of prediction and reward. Science, 275(5306), 1593-1599.
Fiorillo, C. D., Tobler, P. N., & Schultz, W. (2003). Discrete coding of reward probability and uncertainty by dopamine neurons. Science, 299(5614), 1898-1902.
Glimcher, P. W. (2011). Understanding dopamine and reinforcement learning: the dopamine reward prediction error hypothesis. Proceedings of the National Academy of Sciences, 108(Supplement 3), 15647-15654.
Pessiglione, M., Seymour, B., Flandin, G., Dolan, R. J., & Frith, C. D. (2006). Dopamine-dependent prediction errors underpin reward-seeking behaviour in humans. Nature, 442(7106), 1042-1045.


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Transposons, Viruses and RNA interference
My textbook says that in RNAi, a complementary double stranded RNA sequence attaches to an mRNA and silences it using a protein machinery. I Googled and read about this so now I know what siRNA and RISC and microRNA are. But the next thing my book says is

“the source of these complementary double stranded RNA
  sequence [obviously my textbook means siRNA] may be viruses and
  transposable elements.”

What does this mean? Do transposons make siRNA? I thought transposons were non-coding except when they travel via the retrotransposon mechanism.
Do viruses that infect eukaryotic cells donate their own RNA genetic material for the cell to use in RNAi? But I thought RNAi was a cellular defence against viruses, how can viruses help give the dsRNA that’s supposed to fight the viruses? A number of sites online simply state that siRNA is exogenous is origin; do they mean that it comes from viruses?
I would greatly appreciate it if someone could take the time to answer each of my questions one by one or even recommend a site that answers them all.

Transposons and viruses don't "make siRNA". However, an endonuclease called Dicer can process dsRNA from these sources to produce siRNA which is then loaded to the RNA-induced silencing complex (RISC) to suppress propagation of viruses and transposons. The following papers provide a good overview:
Buchon N, Vaury C. 2006. RNAi: a defensive RNA-silencing against viruses and transposable elements. Heredity 96:195-202.
van Rij RP, Andino R. 2006. The silent treatment: RNAi as a defense against virus infection in mammals. Trends Biotechnol 24:186-193.


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What's the difference between Cytoplasmic pool and Granular storage pool?
What's the difference between Cytoplasmic pool and Granular storage pool when speaking about neurotransmitters and synaptic cleft. I encountered this here:

Amphetamine’s mechanism of action
  thus depends on the cytoplasmic, newly synthesized, rapidly metabolized pool of dopamine.
  Methylphenidate’s mechanism of action depends
  on the granular storage pool (Brust, 2004)

Reference
Brust, J. C. M. (2004). Neurological aspects of substance abuse. Philadelphia, PA, Elsevier.

Neurotransmitters like dopamine are synthesized in the cytoplasm and then imported into synaptic vesicles.  When the neurotransmitters are released it is by a fusion of the synaptic vesicle with the neuron's cell membrane, emptying the contents into the synaptic cleft.  Re-uptake of the neurotransmitter back into the pre-synaptic neuron's cytoplasm is done by active transporters, in Dopamine's case by DAT.  The cytoplasmic pool refers to the dopamine in the cytoplasm, while the granular pool refers to the dopamine stored in the synaptic vesicles.


text:
Difference between 'Orbit' and 'Globe' in eye anatomy?
What's the difference between 'Orbit' and 'Globe' in eye's anatomy. Do they refer to the same ? I encountered this in this text:

... ciliary ganglion, which is approximately 3 mm in size, and located
  2-3 mm posterior to the globe and lateral to the optic nerve,...

I've found a rough answer myself:

The globe of the eye, or bulbus oculi, is the eyeball apart from its
  appendages

http://en.wikipedia.org/wiki/Globe_%28human_eye%29

... the orbit is the cavity or socket of the skull in which the eye and
  its appendages are situated. "Orbit" can refer to the bony socket, or it can also be used to imply the contents.

http://en.wikipedia.org/wiki/Orbit_%28anatomy%29

Hi, please don't offer bounties on questions that are 1) Off topic and 2) bad questions. This site is not for medical advice and the question does not give the information needed to make it answerable.

@terdon I understand that the question might not be on-topic or a good question, but offering a bounty could even help this improved. When a question didn't receive any attention, it can neither be improved nor the asker can be trained. There are many options in this website to train people to ask good questions. You even changed the title of two links you provided to sound 'pessimistic'. Instead of comparative commands, I think it would be better if you just train people with optimism and provide the links accordingly.

Well yes, if you think you can improve it edit it. However, personal medicine is very correctly off topic here, we are not MDs and do not have access to the patient. If people base their treatment on our answers, they can cause themselves serious harm. A mod has asked for more information on that question and none has been offered. If this is someone you know tell them how to improve the question. Adding a bounty is not helpful in this situation.


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Calcium concentration in activated dendritic spines?
What are the typical calcium levels reached in single postsynaptic spines following activation of NMDA receptors by an EPSP or backpropagating spike? Everyone seems to refer to that one Neuron paper (Sabatini et al. 2002) which reports experimental estimates of around 1 uM following single synaptic stimulation in CA1 neuron spines. However, most computational papers on LTP (even biophysically detailed models) work with much lower values for Ca2+ transients that do not seem to have concrete experimental support. I am trying to put together a realistic model for hippocampal spine calcium signaling, and would really appreciate it if anyone can point out other relevant experimental papers that provide estimates for spine calcium transients.

An earlier source for an estimate of ${[Ca]_{i}}^{+2}$ in spines comes from hippocampal slices of P13-P19 rats (Majewska et al. 2000). The resting ${[Ca]_{i}}^{+2}$ in this paper was ~80 nM and a back-propagating action potential (AP) elicited a response up to ~250 nM (change of ~170 nM). They included $F_{min}$ and $F_{max}$, the minimum and maximum fluorescence signal from a single AP, as parameters in the equation they used to estimate ${[Ca]_{i}}^{+2}$. This paper may be where the models you mention got their numbers from.
The resting ${[Ca]_{i}}^{+2}$ estimated in Sabatini et al. (2002), where they also used rat hippocampal slices from P14-P20, matches that found in Majewska et al. as it was ~70 nM. For the estimation of the evoked change in ${[Ca]_{i}}^{+2}$ after a single AP they used the maximum fluorescence increase from trains of action potentials at 62.5 Hz and 83.3 Hz as a parameter in their estimator equation, assuming that the calcium indicator was fully saturated at those stimulation frequencies. Their estimate for the change in ${[Ca]_{i}}^{+2}$ per AP was about 530 nM. They then reasoned that the buffering properties of the calcium indicator itself could reduce the change in ${[Ca]_{i}}^{+2}$. Thus they loaded several different calcium indicators with different affinities and at different concentrations, in order to manipulate the $\kappa_b$, the buffer capacity, of the calcium indicator. They observed a very strong linear relationship between $\kappa _b$ and the change in ${[Ca]_{i}}^{+2}$. By extrapolating from a linear fit on these data, they concluded that in the case where there was no calcium indicator in the cell —i.e. when $\kappa _b = 0$— the change in ${[Ca]_{i}}^{+2}$ per AP would be approximately 1 $\mu$M.
So the difference between these studies is that in Majewska et al. they used the maximum observed fluorescence of the calcium indicator in their data after single APs, whereas in Sabatini et al. they attempted to saturate the calcium indicator with high-frequency trains of APs. Furthermore, in Sabatini et al. they attempted to account for the buffering capacity of the calcium indicator itself, thus arriving at a more unbiased estimate.
Reassuringly, later work from the Yuste lab (the same lab as in the Majewska et al. study) could replicate the results of Sabatini et al. when they used similar methodology (Cornelisse et al. 2007). Their estimate for $\Delta{[Ca]_{i}}^{+2}$ for a single AP was also ~1 $\mu$M.


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How are hereditary neural circuits created in the brain during early development?
Whilst our experiences shape the specifics of our brains throughout life, we know that there are a lot of shared properties between us. We all share the same basic layout as, for example, the V1 cortex is always in the same place. Thus it is evident that whilst some of the neural development is experience-dependent, some of it is hereditary/genetic or "hard wired".
It would seem to me that the extent to which the brain is "hard wired" depends on the species. Humans seem to have a lot more room for specialisation in life, whereas some animals don't exhibit much individuality, tending to follow very regular behavioural patterns that have no doubt evolved over time, subject to natural selection.
I have read up to some degree on how experience-dependent development works, but have been largely unable to find any detailed research into how experience-independent development works. That is, how does DNA encode these "hard wired" neural circuits?
Furthermore, the human brain contains some 100 billion neurons. If I assume that maybe 1% of them are "hard wired" into circuits from birth, that's still a billion neurons, each with several connections to other neurons that need to be somehow coded into a DNA sequence which only amounts to a couple of gigabytes worth of data. So how is the complex structure of these "hard wired" (experience-independent) neural circuits encoded in such a limited amount of DNA? How much of the brain is actually hard wired in this way and how much is open to experience-based development? Am I right in associating this process with the phenomenon of "instinct", that is, "hard coded" behavioural patterns in animals which appear to be hereditary?
Is there a name for this field of study? Specifically the study of how neural circuits are generated in the earliest stages, to lay down the high level structure of the brain before experience-based development can take over?

To be as clear as possible. If the brain developed completely independently through experience, then we would all have a different neurological "layout". The fact that the large scale structure of the brain is consistent across humans, and the fact that we are born with certain neurological innate abilities tells me that neural development is subject to the same kinds of morphogenesis processes as the rest of the body, shaping the brain and creating useful circuits before we are even born. My question is, how? How is this information encoded into DNA and how are the circuits created from DNA?

Developmental neurobiology is probably the closest field of study, there's a journal: http://onlinelibrary.wiley.com/journal/10.1002/(ISSN)1932-846X I don't know enough about the genetics really help though.

I will not offer you a description of 'experience-independent' development, as this is not my area, but here is a view on what its limits are. Effectively I am answering:

How much of the brain is actually hard wired in this way and how much is open to experience-based development?

Where a brain area will form is determined by the genotype and the micro-environment that any particular cell faces during development. Or, put in other words, I am not aware of any study showing that experience during development can drastically alter the topography of the brain. The same goes for axons and dendrites of particular cells, although they exhibit higher flexibility after drastic manipulation of experience such as sensory deprivation within the early stages of postnatal development.
This means that inter-areal connections are hard-wired by development in the sense that the target areas of a brain area or particular cell are fixed. As an example, some thalamic neurons are predetermined to target the cortex and vice-versa. A way that experience can influence that fact is by destroying the connectivity between the two areas (e.g. monocular deprivation). But I would be extremely surprised if a study claimed that by some manipulation of experience during development the same portion of the thalamus that normally projects to the cortex now projected to a totally unrelated, distant area such as, say, the brain-stem.

It would seem to me that the extent to which the brain is "hard wired" depends on the species. Humans seem to have a lot more room for specialisation in life, whereas some animals don't exhibit much individuality, tending to follow very regular behavioural patterns that have no doubt evolved over time, subject to natural selection. [...]
  Am I right in associating this process with the phenomenon of "instinct", that is, "hard coded" behavioural patterns in animals which appear to be hereditary[?]

I would challenge you to support this claim by research, as it does not echo anything I know about the nervous system. If anything, primates just have relatively more room for connections in the cortex and the cerebellum even after taking into account their relatively larger brains. Thus, it's not that they are less "hard-wired", in the sense described above, but rather that they have an enormous potential for synaptic plasticity in two key areas of the brain associated with more complex behaviour. When you compare reasonably closely related vertebrates, you find that the phylogenetically ancestral areas are mostly shared and thus their "hard-wired" areas are very similarly connected. Hence, primates only put an extra layer of complexity on top of this ancestral pattern of connectivity by having more space for change.
In conclusion, only the "highways" of the brain are pre-determined during development. The actual connectivity is sculpted by experience. Since the overall layout does not change by experience, animals adapt to their environment mostly through small-scale, synaptic changes.

Is there a name for this field of study? Specifically the study of how neural circuits are generated in the earliest stages, to lay down the high level structure of the brain before experience-based development can take over?

The short answer is the field is called "Axon guidance" as a subfield of developmental neuroscience.  It essentially studies how early neurons send their projections (axons) to their broad target areas where they will make their connections (synapses).  This process is programmed genetically and occurs by itself using "guidance cues" that literally direct their growth through the brain (attracting to some areas, repelling from incorrect areas). see [Ref .1]
After the broad axon pathways are set up, early experience/learning will shape the connections further so that useful ones are kept and non-useful ones degenerate.
It's amazing stuff, check out movies of live axons growing through the early developing brain [Ref. 2]. I was lucky enough to do my Ph.D. studying this phenomenon :)
[Ref .1]: Seminal review of the Molecular biology of axon guidance
[Ref. 2]: Growth of axons figure

This is a cool question and while I'm not a neuro(bio)logist, I've tried to quickly look into this.
Basically what you are asking for is the part of the (human) connectome (this is what researchers call the map/data/... of neural connections), that is hard wired. You may want to take a closer look at the human connectome project, if anyone is going to have/find the answer to your questions, it's going to be them. This paper seems to describe the latest state of the project and this one focuses more on the connection between the connectome and genomics. Sadly both papers are pay-walled and I don't have any access to the Elsevier journals right now, so I can't give you more info than that.


text:
Where does the initial action potential come from?
When talking about action potentials we say that previous neurons caused an action potential in this neuron and that this neuron's action potential caused the same in further neurons.
But what is the origin of the first-ever action potential?
Maybe in a living organism, there are no action potentials initially because the brain is always "on" and some part of the brain can always initiate processes in an other. If that is the case then how is the brain turned "on" initially? If not, then how does the first action potential get triggered from the "resting state"?

The very first evoked spike is most likely triggered by spontaneous activity, as even neurons with no synaptic connections are able to fire action potentials (Luhmann et al. 2016). Later in life neurons can be excited by the external environment through sensory stimulation. At some point the central pattern
   generators also mature and, either by network synchronization or tuning of intrinsic neuronal properties, are able to maintain a self-sustained activity pattern.
The question is then what triggers spontaneous activity during development? It has to do with calcium signaling, both exogenous and from internal stores. The exogenous trigger is paracrine release of GABA and glutamate before the formation of synapses (Rosenberg and Spitzer 2011).


text:
How are cells of the cornea transparent?
We know that cells have mitochondria, chromosomes and other organelles so that's why they are opaque but can you say how the cells present in the eye cornea are transparent and allow light to pass through?

The pupil is a hole, there are no cells. What you probably mean are the cells of the cornea covering the pupil.

Yes i got the wrong term it is cornea

http://www.sciencedirect.com/science/article/pii/S1350946215000488

http://www.practicalfishkeeping.co.uk/features/articles/how-can-glass-catfish-be-transparent it's not totally clear how an entire fish can be transparent rather than white or pink, as the blood should flow in their muscles. check out the cool photo from the above page.

http://www.sciencedirect.com/science/article/pii/S0022519399909487

Most cells are transparent, which is why we can see cells using bright-field microscopy, where the light travels through the cells before you see it. That's how we can see inside onion cells and see structures like onion cell nucleii, moss cells, human epithelial cells and animal mast cells.
The human cornea is made up of five layers, each of which have different structures allowing them to be transparent: the outer and inner epithelial layers are very thin and naturally pretty transparent, and the middle layers have collagen fibres; based on that Wikipedia article, it sounds like there are several hypotheses for why these layers are transparent, but it doesn't look like there's a definitive answer yet.

Actually it is made up of myelin sheath

Collagen is transparent as well --- just look at gelatin. Also, there are no blood vessels in the cornea.


text:
Does sympathetic nervous system acts bilaterally for pupil dilation or other two sided organs?
The question might seem weird. Does sympathetic nervous system acts 'bilaterally' meaning if you shout to a person's left ear a loud noise (e.g. by headphones), will it activate sympathetic system just on the left or on the both sides. For example it will only dilate left pupil or dilate both ?

Yes, they do. At least in the case of pupils. In fact, the absense of simultaneous regulation of the diameter of the pupil is used as a medical test for the evaluation of brain damage.


text:
What Role Antagonists Play in the Study of Drugs?
I am pretty unfamiliar to pharmacology. I'm doing a research on drug abuse, particularly opioids' mechanism of action. I encountered several times evidences that come from studies using antagonists especially naloxone that are to prove something is 'a specific opioid effect':

Opioid-induced miosis in the human ... This action is a specific
  opioid effect as demonstrated by its antagonism by naloxone.

I wanted to know the rationale behind these kind of conclusions. Also an elaboration on the role antagonists play in drug research will be appreciated.

An antagonist is a substance that blocks a particular pathway (a receptor). You can therefore test whether a particular drug acts through the opioid system by using an opioid antagonist. If your substance still works despite the presence of the antagonist (which should block the opoiod receptors), you can conclude that it is not working thorough the opioid system.
Conversely, if your drug is blocked by an opioid antagonist, that is good evidence that your drug works through the opioid system.

What many drugs and compounds do is bind to cell receptors. These receptors then change shape and various things may happen in the cell as a result (including relaying a message to other cells).
Something that binds to a receptor and causes activity is called an agonist. Something that binds to a receptor and causes a partial response is called a partial agonist. Something that binds to a receptor but does not cause activity is called an antagonist as it takes up those receptor sites meaning that nothing else can bind to them and cause and effect.
An opioid effect is one of many effects caused by opioids. Naloxone is an opioid antagonist. It binds to the same receptors as opiates but without causing an effect. If a normal person has naloxone it won't actually cause an effect. If someone who has taken an opiate takes naloxone however, the naloxone will compete for receptor spots, knocking off the opiate and reversing the opiate effect. Also, if someone takes naloxone and then immediately has an opiate, that opiate will not work particularly well as some of those receptors are already taken up with naloxone.
Hope that helps.

Very precise and simple explanation. Thank you so much.

@EhsanAbd No worries!


text:
How can potassium rich foods reduce blood pressure?
How come sodium increases blood pressure, but potassium, which has to some extent similar properties helps lower it?

potassium is really the main guy in charge of everything that happens involving action potentials which in turn govern homeostasis such as blood pressure.
k+ lowers blood pressure due to making it harder to get an action potential going, which in the macro scale causes the heart to pump less.
too much k+ kills the person as it stops the pumping of blood (lethal injections are just lots and lots of k+ along with some pain killing drugs)

This provides some information but does not fully answer the question. Why is $K^+$ the main "guy" rather than $Na^+$.  The question assumes that they have similar properties. In what ways relevant to the question are these two ions different?

I agree with @vkehayas but I'd go a step further to say that this answer is completely wrong as far as the mechanisms for what the OP is asking about. We aren't talking about lethal injection levels of K+ or anything about K+ concentration effects on action potentials when talking about K+ effects on blood pressure.


text:
Do smaller intelligent animals have a higher neuron density to account for their seeming intelligence? Otherwise, what?
It seems like there's a lot of very small animals that have a much higher intelligence than what you would expect if you linearly projected intelligence as a function of brain size. There's ravens, crows and parrots which are much smaller than humans but have a recognizably high intelligence and emotional capacity. Then there's rats and general rodents like squirrels or similar animals like raccoons, and I guess an octopus to throw in which are good at problem solving and fierce fighters. Then there's also bugs like ants which are somehow very versatile and can adapt to many situations despite being that tiny, and with recent information may also have a recognizable emotional capacity like possibly bees.
It would make sense to me if the correlation between neuron density and intelligence isn't linear, but I don't have the information to make any determinations.

@Remi.b You might also consider this and this.

I think the major challenge here is defining "intelligence" in a comparative way. You give many examples which could in their own way be described as intelligence. A better question would be to start with scaling of neuron density across animals. Then get to the question of complexity of behavior.

I mean I asked about neuron density, but for some reason people keep diverting to other points.

@Remi.b - Questions shouldnt be closed if fit for CogSci and Bio. They should be closed if unfit for Bio.

@AliceD Yes, in the post I linked from the meta site (here), I expressed my opinion that CogSci type of question should be off-topic on Bio.SE but as few seem to share this opinion, I happily follow the majority. I retracted my close vote but forgot remove my comment. I will remove my comment now. Thanks

It also may be the case that we are implying intelligence in some cases.
The responses these animals show may have been evolutionarily selected as it best for their survival. However, to us the benefits of these responses may not be directly visible. For example, sheep herding dogs may have a high degree of spatial and numerical capabilities since humans bred them for these traits.

I am not sure it answers the question. The question is about neurophysiology, not about evolutionary pressure or out potential bias to mis-estimate one species intelligence.

I think it is a valid point to keep in mind to explain some things, but you really can't use the rhetoric "it's just pure  instinct" to explain all the results without infringing upon other models or an accepted consensus in biology, at least not without precisely defining the exact mechanisms where this is proven to takes place across every species.

I agree with @RayOfHope that this is a valid point. Misinterpreting instinct as intelligence or considered behaviour would be critical when answering the question of size vs intelligence.

Implicit in the question is the assumption that the examples of the animals you mention somehow would outperform species (with brains) of similar size. Comparing intelligence between different species, no matter how you define it, is going to be challenging.
I would argue that it is impossible to devise a single task with which to compare such different species as ants, octopi, crows, and rats. However some correlations between cognitive capacity and some anatomical features of the brain have been investigated.
Brain-to-body mass ratio
The scaling of the ratio of total brain-to-body mass is not linear. It rather follows a power law relationship, typical to allometric scaling.
$$ m_{(brain)} = \alpha \times m_{(body)} ^R $$
It is convenient to log-transform the mass variables in order to work on the following linear relationship:
$$ log(m_{(brain)}) = R \times log(m_{(body)}) + log(\alpha) $$
The following plot from wikipedia displays this relationship for a number of different species. The slope of this line is $R$, and the intercept $log(\alpha)$. H. Jerrison proposed that the distance of a species from this line could provide an estimate of cognitive capacity. He called that measure encephalisation quotient. The reasoning behind this idea is that of course the brain of bigger animals will be bigger and that of small animals smaller, but is it bigger or smaller than expected from this simple universal model? If so, that may provide a clue for more advanced cognitive skills.

[CC BY-SA 4.0], via Wikimedia Commons
Indeed, we can see as examples that humans and dolphins diverge from this line quite distinctly, which matches with our intuition about these species' cognitive abilities, but so do some species of mice. Is this metric good enough to predict cognitive abilities overall? Given the primitive functions that many brain areas are associated with, such as the brainstem, it is not straightforward that a simple overall increase of brain size above what this simple model would predict, would confer any benefit to the overall cognitive capacity of an animal. At least when attempting to correlate cognitive capacity with several measures based on brain anatomy of non-human primates, it was found that overall (log)brain size or (log)neocortex size are better predictors than the encephalisation quotient. The proportion of brain volume that the neocortex occupies is also able to distinguish the brains of primates from those of insectivores or carnivores. Given the high-level functions that the neocortex is involved with, these results are not surprising.
Neuron size and density
Scaling of the whole brain or the neocortex can be due to a number of things. Either more cells are added, the cells become bigger, more glial cells are added etc. So which is it? According to a 2014 paper by the Kaas group more neurons are added in the cerebral cortex and the cerebellum. This results in a decrease in neuronal density in all species studied except primates, where neuronal density appears to remain relatively stable with the number of neurons. The authors conclude from this result that neuronal size (including axons and dendrites) must have remained stable in primates.

To answer your question, if we take overall brain size or neocortex size as a proxy for the cognitive capacity of an animal, we can conclude that the relationship indeed is not linear, as you predicted. However, we have no reason to believe that some species are exceptionally more endowed than what would be expected of them based on brain size given this non-linear relationship, except perhaps primates. Of course comparing mammals to invertebrates based on this evidence is a non-starter as they lack a centralised brain and/or neocortex.
Although we may be surprised by the remarkable things some species can do, this may only mean that we have not looked close enough at the capabilities of other yet unsuspected species. Conversely, our amazement may simply be because of the fact that we underestimate the capabilities of animals that are not similar to us.
Further reading: Evolution of the brain and intelligence, G. Roth and U. Dicke, TICS, 2005.10.1016/j.tics.2005.03.005
Related questions in Biology SE:

Is there a correlation between total neurons and intelligence?
Is the ratio Brain Mass/Total Mass still considered a valid indicator of intelligence?


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What are the safety precautions I should take if I want to experiment with C. elegans (at home)?
Caenorhabditis elegans (C. elegans) is a nematode (roundworm), and many nematodes do infect humans and cause diseases.
How much is C. elegans safe (or unsafe) in this respect?
C.elegans is a popular model organism, but is it safe to experiment with it at home? Or risk of infection shall outweigh desire and interest for home science?

Caenorhabditis elegans is completely safe, it is a soil worm not parasitics. you can google the name if you don't believe be.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/