text:
Why don't we hear ultrasonic sounds as aliased versions of the original signals?
The upper limit of hearing is approximately 15 kHz, dependent on age and other factors. According to the principles of digital signal-processing, such an upper limit would mean that the auditory system samples at least at 30 kHz or more.
Now suppose an ultrasonic signal, say a 40-kHz acoustic frequency - why would I hear nothing, instead of that signal aliased at a 30 kHz sampling rate?

In order to hear a sound of a given frequency, you have to sample at twice that frequency (really, above twice that frequency). This is the Nyquist rate. Not sure if you're interested enough, but this Youtube video on the concept is really good: https://www.youtube.com/watch?v=yWqrx08UeUs

When a digital sound is processed by a speaker, the speaker diaphragm travels through every point in space between the two digital bits of data. therefore, all sounds transmitted in air are generated and heard non-digitally, they are continuous signals limited by atomic size, which is bigger than HDD requirements. Frequency is mathematical, but the human cellular ear structures are not mathematical so you can't rate an ear in mathematical way very clearly.

The answer to your question is in here. I scanned through it, but I don't have time right now to write up a formal answer (someone else is welcome to if they would like). Short answer is that, according to this, the exact mechanics of sound perception are still not pinned down, but it likely has something to do with a lack of space within in the cochlea since vibrations at different areas correspond to the perception of different frequencies.

I don't have time to type up a whole answer right now, but the premise of your question has a major flaw: the Nyquist rate that you are referencing by talking about necessary sampling rates applies to discrete sampling of a waveform; this isn't how auditory information is represented in the cochlea or auditory nerve or anywhere in the brain that we know of, so it does not apply. You could look into "phase locking" which occurs at lower frequencies, but higher frequencies can just as easily be represented by their envelope, or phase information can be distributed across a population.

@BryanKrause I would like to see your entire answer later. It is a conceptual simplification but there are discrete aspects to how sound is received and encoded, at least potentially: since frequency is tonotopically represented, and the spiral ganglion has fibers that innervate different sections of it, they could potentially be 'sampling' that section of the basilar membrane even though the entire waveform is complex and excites many places on the cochlea.

@BryanKrause The auditory nerve conserves that tonotopy: http://images.slideplayer.com/18/5700795/slides/slide_38.jpg
Relatedly, the actual auditory neurons fire discretely, e.g. at a certain rate, not continuously, and presumably some aspect of auditory perception is limited by the max rate (~1 kHz) although this could be overcome by groups of neurons (volley principle).

@kingfishersfire I have found that page before and love it, thank you for reminding me of its existence. It's getting bookmarked.

@Bzrs I am quite familiar with tonotopic organization of the cochlea and auditory nerve, my point is that this has NOTHING to do with the sampling rate. You can have a part of the cochlea respond to 50kHz tones (humans don't, but mice do, and vocalize in that range), but no need to fire at 50kHz. Also although action potentials are (roughly) point processes, that is not the same as discrete sampling...

...Discrete sampling  of a point process would imply you have a series of 0s and 1s, but an action potential, even though it is a point process, can occur at any arbitrary time point: even if your maximum firing rate is 1000 Hz, you could have a spike at t=0s, or t=.001s, or t=.0001s, or t=.00001s. This is actually a necessary concept behind the "volley principle" you mention. At the highest frequencies, there is no evidence for volley principle, instead cells sensitive to basilar membrane vibrations in the high freq area spike w/ respect to the amplitude of those vibrations, not phase.

@BryanKrause I get what you are saying, just a few points: (1) detection of up to 90 kHz has been reported in humans through bone conduction, see https://www.ncbi.nlm.nih.gov/pubmed/2063208 (2) amplitude would seem to be a poor way to code high frequencies given their greater attenuation....

For echolocating animals which hear well into the hundreds of kHz it seems particularly problematic. I doubt you could get large displacements of the BM in response to high frequencies without help (active amplification), but immunogold labeling has shown similar amounts of prestin in the base and apex which seems inconsisent with amplification being more important at the base. https://www.researchgate.net/publication/44651053_The_ultrastructural_distribution_of_prestin_in_outer_hair_cells_A_post-embedding_immunogold_investigation_of_low-frequency_and_high-frequency_regions_of_the_rat_cochlea

Let us continue this discussion in chat.

Short answer
The cochlea is a tonotopic map with certain physically determined boundaries that determine the range of frequencies perceived. Ultrasonic soundwaves simply do not have a correlate on this map.
Background
The cochlea is a frequency analyzer that basically translates acoustic frequencies into a place-map. High frequencies are encoded basally (up to 20 kHz), low-frequencies apically (down to 20 Hz or so). Hence, it is pretty much a Fourier analyzing system (Fig. 1). This way of analyzing sounds is referred to as the place-coding theory of pitch. The place where a frequency is encoded is mainly dependent on physical characteristics of the basilar membrane in the cochlea. Every part is sensitive to a slightly different frequency then the next. This is caused by gradual variations in the stiffness and width of the basilar membrane, among other less important factors like hair cell length and so forth. The specific physical characteristics determine what specific resonant frequency a particular part of the basilar membrane has. Hence, incoming sounds are torn apart with standing waves, where each frequency results in a standing wave at a particular spot in the cochlea.

Fig. 1. Tonotopic map of the inner ear. source: Ternopil State Medical University
The frequencies mentioned are physical wavelengths of the acoustic air pressure differences entering the outer and middle ear. The cochlea translates these into fluid-based pressure differences. Hair cels in the cochlea pick up these fluid pressure differences and tranlate them into potential gradient differences.
The sampling rate of hair cells is pretty much infinite, as they work on a continuous membrane voltage, i.e., they are analogue.
The secondary neurons, the spiral ganglion cells, translate these voltage differences into neural spikes and lead them through the auditory nerve to the brain.
Neural spiking follows the acoustic frequencies up to, say 1 kHz (frequency following response). This phenomenon is referred to as the temporal code of pitch hearing. After that, the refractory characteristics cause single fibers to fire only to one in a few wavelength periods. So at the upper limit of hearing, say 20 kHz, a ganglion cell may only fire once every 20 wavelengths or so. No problem, as many others do the same thing. Stochastics cause the wavelength to be nicely encoded in a population of responsive fibers. Furthermore, the auditory cortex contains a tonotopic map, meaning that high frequencies are processed elsewhere then lower frequencies. In other words, the auditory nerve doesn't need to faithfully encode the incoming wave.
A nice example in this are cochlear implants; they stimulate the auditory nerve with electrical currents. The place of the electrodes determines the pitch, not their pulse rate (although it can have an effect).
Now why are you not hearing ultrasounds? Simply because the basilar membrane does not contain regions sensitive to frequencies above 20 kHz or so. This is referred to as the Greenwood map, which depends on species.

Thanks for the answer. Just a few questions: re: "The sampling rate of hair cells is pretty much infinite, as they work on a continuous membrane voltage, i.e., they are analogue" don't they have to depolarize, though, which is a discrete event? Is your statement that there is no real limit at all related to this study which showed that OHCs are not limited by their membrane time constant? https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3143834/

@Bzrs The point is that hair cells voltage is continuous - those cells don't fire spikes. So, no, depolarization is not a discrete event. The most likely explanation is that mechanical deflection of the hair cells causes a channel to open; that open probability is a function of the magnitude of the deflection. The depolarization is analog meaning that it is continuous. You could depolarize by 1 mV, or 2 mV, or 0.5 mV, or 0.1 mV, or anything between. Here we are talking about the inner hair cells, the primary sensory cells, not the OHCs.

@BryanKrause I know IHCs actually transduce the sound, just was thinking there would have to be a similar mechanism behind their analog quality and it appears that there is (it being the probability of open channels). It's a bit confusing to me since one could see discreteness in some aspects of this, e.g. neurotransmitter release from the IHC is also continuous/analog due to channel state being so, but the release itself is quantal (released in packets of constant quantity) according to "Neurotransmitters and Synaptic Transmission" by Sewell in "The Cochlea" (Springer Auditory Handbook).

@Bzrs Yes, there are some aspects that are still somewhat discrete, like neurotransmitter release, but even that is continuous on average: see law of large numbers. Essentially, the membrane potential is setting a probability of release, and release events are frequent enough that the output is roughly continuous, especially because there will be some postsynaptic temporal filtering that smooths the individual release events.

@Christiaan if freqs above 20 kHz have no representation in the human cochlea, what is your interpretation of the human ultrasound via bone conduction studies? This study claims to rule out lower freq stimulation (https://www.ncbi.nlm.nih.gov/pubmed/23384569) and another by the same group shows inhibition of tinnitus after 30 kHz BCU, which they say is evidence that their BCU stimulus activated the cochlea base (https://www.ncbi.nlm.nih.gov/pubmed/24530434). Your answer http://biology.stackexchange.com/a/27901/28436 invokes ossicles and not cochlear representation as the limiter on high freqs.

Also, some interesting findings: BM motion of up to 100 kHz detected in guinea pig, despite it being well over the upper freq limit for them: https://www.ncbi.nlm.nih.gov/pubmed/16603325
Responses of up to 100 kHz recorded in single OHCs: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC16347/
Presumably the analog/continuous voltage changes induce conformational changes in prestin particles such that the OHCs can change length at this rate. Perhaps, as with volley principle, there are enough prestin particles that only a subset need to be shrinking/enlarging to cause movement each cycle?

Why should the OHCs amplify at such high rates (essentially following a 100 kHz signal) if detection at this high frequency will only matter on the place code? At this point we are obviously butting against the limit of knowledge on the topic, but...it's fascinating stuff.

Sorry, final comment: the OHCs amplifying 100 kHz signals is not inconsistent with the place code. Rather, it serves to boost the strength of the response which is likely needed for high frequencies. So its purpose is not encoding frequency so much as it is amplifying the signal; and failing to keep up with the high frequency would cause distortion through subtraction/addition (similar to what is posited for prestin's mechanism of conferring frequency selectivity).

@Bzrs  Per this answer: http://biology.stackexchange.com/a/27901 , "the transfer function of the ossicle chain in the middle ear is a suspected culprit in setting the upper frequency limit to 20 kHz (Hemila et al., 1995)." The answer has a link to that paper. So... we have a 20kHz LP filter in the acoustic path to the hair cells; even if the latter were doing "sampling", we still wouldn't get aliasing. otoh, bone conduction bypasses the middle ear, explaining how we can "hear" ultrasonics by that path.

@JamieHanrahan The ossicles do not set the upper frequency limit. That's an outdated idea. See http://www.pnas.org/content/99/20/13206.full.pdf

I think that you are misquoting Aliasing.
Digital acoustics is explained in a mathematical sense, Aliasing is a maths concept. Real life acoustics is explained in a physical sense, which talks about reflection, absorption, phase change, harmonic modes, weights... the perception of sound is discussed as psychoacoustics and cortical structures and individual nerve impulse detection thresholds. consider for example the explanation of drum acoustics, it is not digital and on no physical objects will you see the word "Aliasing" used: https://en.wikipedia.org/wiki/Vibrations_of_a_circular_membrane
Aliasing refers to a digital concept, whereby we devide screens into pixels, and you can't make out objects narrower than a pixel. A wave is at least 2 "/////" points of data, so it requires a 2x window so we have 44k CD's to code 22Khz sounds.
I'll just tackle this precise question, aside from the mis-use of the term Aliasing: why would I hear nothing instead of the signal aliased at a 30 kHz sampling rate?
Pressure waves are continuous and physical sounds... A continous sound or physical object can't be subject to the digital distortion effect "Aliasing" which for example refers to the generation of infinitely high frequencies in between two sampled points of a clock rate...
Because physical sound is continuous, it can't have frequency distortion related to it's sampling rate of 15/30 Khz, it can attenuate and physically react with physical objects including other sound pressure waves and cause physical objects to resonate in different modes of movement.
The sound detection depends on the physical excitation of hairs and nerves that must exceed a threshold of detection. physical objects don't have radical and odd excitation modes when they absorb a frequency that is too high, they can resonate in different modes, but they wack about wildly and produce volume clipping and sound artefacts. Most of the time they don't have a limit of frequency after which they go crazy. the closest you can get to strange frequency modes in physical objects is resonance where the movement builds up into a high kinetic movement like the Tacoma Narrows Bridge. You have to approach the ear as a physical model and not a digital one. I think of the resonant modes of structures in the ear similar to a guitar string or a gong moving in 3D space. This gives you an idea of the nerve signals in the ear:
https://www.youtube.com/watch?v=1JE8WduJKV4&t=17s
Almost all sound that is detected inside an ear is distorted by reflection from it's initial shape and source, and thereby it is smudged into reverb similar to light travelling through frosted windows.
Human brains and tissues are not digital and quantized, they aren't even analog, the are cellular with different types/sizes of receptor cells and nerves, variable and organic. You can say they alias only when you talk about perfectly equal sized cell matrix in 2d/3d pattern, like photoreceptors, except that our minds disregard information on cellular scales that aren't useful to us, like a biological version of aliasing would be.
If you study the function of the cochlea you will find that the structures, hairs, membranes are so different from a digital aliasing concept.
Human ears collect high frequency sounds unlike the dished ears of bats and cats and dogs, which are made of stiff cartilage that reflects higher frequencies well, into the ear canal. high frequencies are absorbed very fast by the skin and it takes specialized organs to reflect them to stiff cartilage chambers lined with hairs, each part of which is adapted to further reflect and absorb different frequencies.
The cochlea is organic and cellular, and it is similar to multiple electret microphone diaphragms and cilia all existing inside a complex organ which sends the vibrations to nerves. Sounds have to be collected by dishing and focused onto light and rigid membranes.
There is very much artifacting from all frequencies as they reach the ear. The sounds reflect of different surfaces, although high frequency ones absorb more easily and therefore are heard more linear from the source to the sensor, and have more time precision and more binaural precision.
Sounds don't tend to be generated in the exact same spot(point sources), so if you have for example an insect generating high frequencies, it will make a complex wave shape, that excites a large envelope of air around it, like dropping 5-10 stones into some water, and the outgoing wave will not be a simple form, but a complex series of phase interactions similar water that is excited by a swimmer. In that sense it has some properties of a moiré pattern, but it isn't aliasing, it's complex wave and phase interaction.
An Aliased oscillator on the other hand is a digital sound which contains infinitely high frequencies, because digital encoding forces sudden changes in amplitude to be abrupt, which is different to nature, where sounds are continuous and not discrete sets of values.
As sound travels through air and through flesh, the high frequencies which are all pure sine wave components of the overall sound, will simply be attenuated according to complex spectra of attenuation which correspond to the ambient air conditions, the angle of incidence towards the reflective and transmitting ear vestibules.

Nice answer, but can you add a couple of references or a good textbook to provide support/further information?

I don't know that I understand what you're saying some of the time, but from your analogies I would guess you come from a visual background.
Human ears also have cartilaginous pinnae that help amplify sound. The cochlea is not lined with hairs (did you mean hair cells?). And with regard to high frequency sounds, the place-code of the cochlea does come with particular frequencies being represented in a particular place.
I know the ear is not digital and that signals do not come in without a lot of modification. It's a simplification, but my question was conceptual.

You can actually bypass the entire impedance from air to fluid/ossicle transfer function aspect of it if you transmit a signal through bone conduction, and indeed studies show that people (even the deaf) can hear higher frequencies this way. In which case the limitation may not be pre-cochlear.
https://www.ncbi.nlm.nih.gov/pubmed/2063208
https://www.ncbi.nlm.nih.gov/pubmed/11234768

This answer makes some good points but a lot of the details are misleading or wrong, especially the comparisons between human and other animal hearing. I think it would be greatly improved if @comprehensible was able to source the real stuff and remove anything they can't find sources for.

Bzrs,that study talks about brain implants of some kind, ultrasound hearing aid cortical implants. Cats can and bats can hear above 60Khz. they have forward pointing ears with round dish structures that point towards the ear canal. some primates have dished ears, but almost all the human ear convex shape points away from the inner ear. The major mistake in the text is that i have not considered how the human auditory cilia can react to signals of 15Khz in a way that can be compared to a digital encoding of 30Khz which is necessary to detect a peak and trough at 15Khz.

Most of my understanding of sound is from many years of backwards engineering digital audio synthesizers, and knowledge of physical modelling in audio, reverb, direct versus indirect audio. Vibration modes of a gongs and drums and the function of speakers and microphones. Most of the information is so obvious to me, that the human nervous system doesnt have a digital clock rate at 44khz, or a binary function, you have to tell me what i have stated too vaguely so that i can reference it.

@comprehensible "Human ears collect high frequency sounds unlike the dished ears of bats and cats and dogs" - All of those non-human animals hear at higher frequencies than humans. This has to do with the physical properties of the cochlea, not the pinnae. "The sounds reflect of different surfaces, although high frequency ones absorb more easily and therefore are heard more linear from the source to the sensor, and have more time precision and more binaural precision." - The logic here is incorrect, and I'm not sure what point you are even making.

@comprehensible "High frequency sounds don't tend to be generated in the exact same spot" - By "exact same spot" I think you mean "precise frequency" - however the OP isn't talking about natural sounds necessarily, and it is certainly possible to artificially present tones fixed to any frequency. And your last paragraph is mostly jibberish, there is no difference in the "pureness" of sine waves at different frequencies, and probably the head itself is the main attenuation source, allowing for sound localization based on interaural level differences.

High frequencies are absorbed more readily by air, trees, stone, the ground, water, etc. they don't travel so far. that's simple. what that means is that the higher pitched the sound, the more likely that you will not have heard it as an Nth reflection... Aliasing is a kind of distortion, and indirect hearing is a temporal and spacial distortion, so I thought it was relevant to try and explain that.... Animals have reflective objects surrounding their ear, which transmit an imprecise reflection of the sounds, and it further illustrates that we have temporal and phase distortions, not Aliasing.

You presume that i mean Frequency when i say "generated in the same Spot" ? I mean Point Source of sound that doesnt exist in nature. you presume Gibberishly yourself. Your judgement of giberrish seems to arise from a mind that doesnt even understand the concept of a "point source" of sound, you are confused. You need to consider that SOUND SOURCES aren't really idealised point sources. Depending on the application, you can shape speaker(s) so you have cylindrical waves, or dipole waves, or sections of a monopole wave ..., or a combination of several patterns.

I'm sorry, you're right, it was dismissive to say gibberish, I apologize. What I meant to say was that I don't think your points actually go toward answering the OP, because the OP was talking about tones, and in that context it doesn't matter what naturalistic sources of sounds are: I totally agree with you that pure tones are not directly relevant to natural hearing. There are still misunderstandings by the OP that are more relevant to answering the actual question.

Sorry for not writing it more sensibly. Having programed anti-aliased oscillators and studied physical acoustics, I was confused by the question and it left me in a state of incomprehension when i tried to interpret the wording. I have rewritten paragraphs 3/4 to take up and answer his question properly.

I actually think I realized the answer this morning. The biological equivalent of 'sampling' should occur at the neural level, e.g. after successful transduction. Since properties of the basilar membrane (e.g. stiffness/thickness) AND the transfer function of the ossicles would need to allow passing of a high frequency sound into the cochlea prior to sampling, the excessively high signal may never make it there in the first place.

I would agree with what you've said about the properties of the ear, but I'm not sure that the concept of sampling is a good fit on a neuronal level either. Though I would be very interested if you had some info about how it would relate.

I just found this and will be digging into it as best I can with my limited neuro background:  http://audiology.pagesperso-orange.fr/en/cochlear-sampling-theory.pdf

Also, not sure if you saw my answer above, but considering the nature of spiral ganglion fibers innervating different places along the cochlea, and the tonotopic representation of frequency, there's at least potential for these to act as 'channels' which are sampled/filtered/processed in different ways. This was obviously the thought behind some cochlear implants but I admittedly don't know how much it is an accurate reflection of the biological ear.

This looks interesting. Thanks for sharing. It looks like our supposition about the limits of the cochlea may have been premature.

From what I can gather from skimming the paper is that there isn't a practical limit to high frequency detection. The multiplexing that is proposed (p. 53) that got us to 15-20 kHz could get us much higher. Though it seems like the paucity of cochlear space devoted to higher frequencies means the cochlea has a functional high pass filter. Fascinating paper though, I'm going to dive into it later when I have more time!

Yeah, that 'multiplexing' is essentially the volley principle as explained in the link you provided above. It does not satisfactorily explain the hearing of other mammals, however, such as echolocating bats and whales. To hear 200 kHz you'd need 200 IHCs responding (to be strict) or else have enough of them firing such that the brain could still reconstruct the signal from the incoming periods (e.g. for a 10 Hz signal you wouldn't need firing on all 10 cycles but if you got 1, 2, 5, 6, 9, the brain might still deduce the frequency). Harder with 1, 3, 5, 7, 9, though (would look like 5 Hz).

Multiplexing and volley principle is not necessary for detecting or perceiving sounds; phase information is not needed to perceive a sound at a particular frequency, only amplitude. There is no need for the brain to be able to reconstruct the exact waveform of an incoming sound to be able to perceive it, a spectrogram is almost certainly sufficient. Phase information is important for localization of low frequency sounds, however, so it is still important, just not necessary at all frequencies.


text:
How did the felines get to America?
I don't know if the felines got originated on America or on Africa, but I do know there are species of cat in America and Africa that belong to the same family and genus (Felidae & Panthera).
How did the evolution of these animals beat the vastness of the ocean? The same way as Homo sapiens? Or did they coexisted before Pangea split?

There are species of felines native to Eurasia, so it's not as though there is a great gap, either geographically or genetically.

Short answer
It is believed that low water levels occurring several times during the last ten million years facilitated migration and divergent evolution of the felids. The North-American ocelot, lynx, puma, leopard cat, and domestic cat are believed to have evolved from a common ancestor that crossed the Bering land bridge between 5 to 9 million years ago from Eurasia. Note that Pangea broke apart 175 million years ago, way before the Age of Mammals even started, 65 million years ago.
Background
It is believed that modern felids arose in Asia with the divergence of the genus Panthera 10.8 million years ago (Mya) and the bay cat lineage 9.4 Mya. These dates correspond to the low sea levels that occurred during the late Miocene (Fig. 1). Between 8.5 to 5.6 Mya a progenitor of the caracal lineage arrived in Africa. The common ancestor to five felid lineages (ocelot, lynx, puma, leopard cat, and domestic cat) migrated across the Bering land bridge to North America, referred to as the New World migration. This period is also believed to have facilitated migrations of the Eurasian carnivores (ursid, procyonid, mustelid, and saber-toothed felids) to North America.
Additional Pliocene/Pleistocene migrations paved the way for the differentiation of the cheetah, originating from the North American puma and migrating to central Asia and Africa. Reversely, Asian Panthera species spread into America (jaguar, lion) and subsequently into Africa (lion and leopard).

Fig. 1. Global migrations of felids. source: Johnson et al., (2006)
Reference
- Johnson et al., Science (2006); 311: 73-7

I thought modern domestic cats were originally bred from wild cats of Egypt and the Middle East.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


text:
What is the highest range mosquito can be detected via Microphone?
Just wondering when a mosquito attack at night I can hear it around my head, shoulders upper corps. Is it any statistic how far our ears or a microphone could detect it is nearby?

In accordance with the article Using mobile phones as acoustic sensors for high-throughput mosquito surveillance mobile phone microphones can detect moscitos in 10 to 100 mm range (depends on a model). In an empty room mosquito can be detected at approx. 3 m (Sound Pressure Level).

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


text:
Where in the cochlea are frequencies below 200 Hz detected?
I understand that different frequencies are detected in different positions along the cochlea.
I'm also aware that the range of human hearing is roughly between 20 Hz and 20 kHz.
However, looking at the below diagram, the lowest frequency, at the end (apex) of the cochlea, 200 Hz is the lowest frequency.
Hence the question: wwhere or how are the lower frequencies (between 20 Hz and 200 Hz) detected?

The answer is two fold, each related to the two ways pitch is encoded in the inner ear. These two mechanisms are place coding and rate coding.

Regarding place-pitch; given that there are hair cells tuned to frequencies lower than 200 Hz, it's not surprising that your linked image is incorrect. Below are 2 (random) figures drawn from the internet showing the human tonotopic map that do show the lower frequencies:

Regarding rate-pitch: at low frequencies, say from 1 kHz and below, the auditory nerve is more and more able to phase lock onto the stimulus. Because of the refractory period of auditory nerve fibers of a few ms or so, this process becomes more pronounced at frequencies below, say, 500 Hz. In guinea pigs phase locking (e.g., Stronks et al., 2010) becomes apparent at higher frequencies than in humans. This rate pitch coding still is most pronounced at the place where the frequency of the tone stimulus matches the characteristic frequency in the cochlea, yet because of the high frequency tail (see the other answer from Bryan Krause), it may occur at other places as well at high stimulus levels. Phase locking is thought to contribute to pitch perception, although it's a matter of debate.

In cochlear implants, for instance, rate coding could be easily implemented, yet in most systems speech coding is based only on frequency mapping based on place-coding by placing electrodes at the corresponding frequency bands in the cochlea. Cochlear implants, in a nutshell, bypass the degenerate hair cells in severe-to-profoundly deaf ears by directly stimulating the auditory nerve. They consist of an implanted array of electrodes in the cochlea (for place coding), and an external speech processor converts speech into a number of frequency bands equal to the number of electrodes to be able to place-code different frequencies along the tonotopic cochlear map.
Reference
- Stronks et al., Hear Res (2010); 259(1–2): 64-74

Fig. 1. Human tonotopic map. source: Cochlea.eu

Fig. 2. Human tonotopic map. source: Abdulla, Audio Watermarking for Copyrights Protection, 2007

A figure like this is likely representing the best frequency for hair cells. In actuality, cells respond to a broad range of frequencies. Perceptual specificity comes thanks to lateral inhibition. Tuning curves look something like this:

image from: http://www2.tulane.edu/~h0Ward/BrLg/AuditoryTransduction.html
The y-axis here is in units of threshold, so a small number means the cell is detecting quieter sounds at that frequency. For example, cell D here has a best frequency around 300 Hz, but was still somewhat sensitive to the lowest frequencies presented (looks like about 180 Hz). You won't see many experimental tuning curves that go below that because a typical speaker doesn't go down that low.
If someone says humans can detect sounds down to 20 Hz, that doesn't necessarily mean any inner hair cell has a best frequency at 20 Hz; if it did, it would probably be somewhat sensitive to some even lower frequencies, too, and you'd have to report a different number. If humans can hear 20 Hz sounds, that just means that for some cell, 20 Hz is on the far left end of its tuning curve, such that a loud enough sound at 20 Hz can be perceived.
You can assume the cells most sensitive to the lowest frequencies are at the apex.

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


text:
What is splice junction pairs?
Splicing is a modification of pre mRNA when all introns are removed and exons are joined.
What is a splice junction pair? It is two exons which connected together?

Splice junctions are the exon-intron junctions, at which splicing takes place.
Splice junction pairs are the pairs of such junction (to cut an intron you need to splice in two junctions).
So, you are almost there, since two exons will be joined in correspondence of two subsequent splice junctions.
You might find these slides useful (slide B-6)

EDIT:
As Adam pointed out the slides are no longer available. I have no idea on where they are gone, but I suggest referring to the following wikipedia pages for an introduction:
RNA splicing
Exon junctions
Alternative Splicing

The slides are no longer there (Page Not Found, 404)

Added some very basic new references (wikipedia). I don't know where the original slides went!

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
Energetics and Products of Pepsin/HCl Protein Digestion
What are the energetics of protein digestion during which the enzyme pepsin is "activated" (whatever that means) by HCl?  I've looked and been unable to find anything like a chemical equation that includes an energy term.
Of course, pepsin, being an enzyme, is not used up in that sought-for equation.  Is HCl used up?  If so, what are the products?  How and in what form is the chlorine removed, assuming the HCl is consumed in the equation?

This is well-explained on the Wikipedia page for pepsin. You are misinterpreting the use of the word activated. The protein is secreted by chief cells in the gastric glands in the form of pepsinogen, an inactive pro- form which has an extra ~40 amino acids at its N-terminus (the propeptide). The propeptide binds at the catalytic site of the enzyme and keeps it inactive. At low pH (this is where the HCl comes in - HCl secreted by parietal cells of the gastric glands acidifies the stomach) the protein is able to cleave off its own propeptide, making it fully active.

So it would appear that the HCl is consumed in a chemical equation that looks something like:
pepsinogen + HCl => pepsin + ?Cl + ?Joules
Moreover, the HCl apparently isn't substantially involved in digesting the protein directly (say, by hydrolyzing it).
Furthermore, pepsin isn't consumed in the chemical equations for digestion (it being an enzyme) so much as it is lost due to normal mechanical effects.  So my question really reduces to filling in the '?' in the prior equation.

The HCl isn't really involved in the reaction at all, except in the sense that it drives the pH down. There may be some binding and/or release of protons during the autocatalytic process. I haven't been able to find anything about the free energy change that accompanies the reaction. Of course the entropy will increase (1 molecule > 2 molecules), so it is even possible that the enthalpy term (your ?joules I assume) would be positive.


text:
Do clients of cleaner fish queue up?
I can't remember if I saw it in a cartoon, a documentary, or both, but the notion is that the clients of cleaner fish wait in line to be cleaned. "Clients" means the fish (or other aquatic animals) who are cleaned by cleaner fish.
I tried to find a study whose sole purpose is to confirm that client fish wait their turn to be cleaned by cleaner fish, but I only found articles that seem to refer to this while studying other cleaner fish behaviour.
Statements I came across that support the notion:

Most photographs of fish in coral reef are at cleaner stations because the fish are waiting there which allows photographers time to photograph.
Cleaner fish "have a positive impact on local reef fish diversity", which could imply many different fish come and may not attack each other to benefit from the cleaner fish. This one's more of a stretch.
"Others wait no longer than 30 seconds before searching for cleaners elsewhere." The source is German, so I can't go deeper.

Do fish wait in line to be cleaned by cleaner fish?
Side question: Is this an example of reciprocal altruism?


text:
Why do classic psychedelics not cause withdrawal, despite high tolerance?
"Classical" psychedelics, such as LSD, DMT, and Mescaline, are serotonin agonists that cause hallucinogenic effects. They are notorious for having rapid tolerance, such that after consuming such substances, one would need to (at least) double the dose to feel the same effect if taken daily. No other substance, not even opiates, have such a high tolerance curve.  While this tolerance contributes to the less-addictiveness nature of psychedelics, there is no observed withdrawal. Furthermore, because of the high Therapeutic Index, some users may consume large doses.
Wouldn't such tolerance result from 5HT downregulation, and therefore cause withdrawal? Is it something with serotonin, or is the mechanism different?
There is evidence that 5HT downregulation is what actually causes the effects of anti-depressants. This explains why it takes a few weeks for SSRIs to kick in. Perhaps, this explains why psychedelics can have an antidepressant effect? Perhaps, unlike other neurotransmitters, activation and downregulation of 5HT is not harmful?
https://www.ncbi.nlm.nih.gov/pubmed/7972628

I would say it is very debatable if those drugs are non-addictive and do not cause withdrawal. (Also, withdrawal is not "just" a physical effect.)

@Remi.b the question core is all about tolerance, in turn boiling down to the [down]regulation of neurotransmitter-receptor systems. This is perfectly ontopic here imo.

Short answer
Withdrawal effects are generally associated with drugs that induce feelings of euphoria by stimulating the reward center of the brain, either directly (cocaine, morphine) or indirectly (alcohol, nicotine). The classic hallucinogens have little effect on the dopaminergic pathways and hence do not cause serious withdrawal effects as observed with other classes of psychoactive drugs.
Background
Withdrawal is defined by the WHO as:

a group of symptoms [that] occur on cessation or reduction of use of a
  psychoactive substance that has been taken repeatedly, usually for a
  prolonged period and/ or in high doses.

The typical drugs that are associated with withdrawal are alcohol and other sedatives, opioids, and stimulants.
Alcohol and sedative withdrawal can lead to anxiety, agitation, and depression. Opioid withdrawal results in drug-seeking behavior that may continue after the physical symptoms have abated. Stimulant withdrawal (the ''crash") is associated with depression, malaise, inertia, and instability (source: WHO).
All these characteristic symptoms are basically caused by the fact that the nervous system counteracts the drugs effects and downregulates the receptor systems activated by the drug. Therefore, more and more of the drug is needed. Indeed, downregulation is one of the physilogical mechanisms underlying tolerance (Stewart, 1993):

Tolerance refers to the decreased effectiveness of a given drug with repeated administration.

There are many factors underlying tolerance. For example, there is acute, short-term tolerance seen with cocaine use, but also a long-term tolerance form example seen in opioids. One factor in developing (long-term) tolerance is a downregulation of the receptor systems involved. Alcohol and other sedatives target the GABAA system. GABA being the primary inhibitory neurotransmitter in the central nervous system, it's not surprising that abstinence in a situation of tolerance results in over-stimulation of the nervous system (anxiety, agitation). Likewise, opioid tolerance results in mu-opioid receptor downregulation (Stafford et al., 2011). Given that mu receptors mediate positive reinforcement following direct (e.g.., morphine and other opioids), or indirect (e.g., alcohol, cannabinoids, nicotine) activation it is readily apparent why opioid abstinence results in the craving for the drug, as it is thought that after prolonged use, the user is unable to experience pleasure without the drug. At this point, the person is addicted (source: The Treatment Center). According to the NIH

Addiction is defined as a chronic, relapsing brain disease that is characterized by compulsive drug seeking and use, despite harmful consequences.

Now we come to the conclusion that dopamine is central to addiction, also for drugs not directly activating it, such as alcohol and nicotine. The latter group indirectly release dopamine in the brain's reward center (the limbic system).
The classic hallucinogens stimulate the serotinergic system, and specifically the 5HT2A receptors (López-Giménez, González-Maeso, 2017), but fail to activate the reward centers in the brain. Indeed, all addictive drugs activate the reward circuitry of the brain, thereby producing the subjective “high” that the drug abuser seeks (Gardner, 2011). Tolerance to these drugs has rarely been reported (Smith et al., 1999) and LSD  rarely produces serious withdrawal symptoms (source: LSD Abuse Help. But in rare cases, tolerance can develop and is associated with 5HT2A receptor downregulation (Gresch et al., 2005) and the development of hallucinogen persisting perception disorder (HPPD). An LSD tolerance can be developed quickly, although it usually dissipates within just a few days depending on the user, their dosages and frequency of use. Long term tolerances are uncommon because users do not frequently repeat doses of LSD without taking breaks in between (source: Hallucinogens).
The SSRIs you mention basically work by downregulation of presynaptic 5HT1A receptors (Celeda et al., 2004), which are unrelated to the effects of hallucinogens.
References
- Celeda et al., J Psychiatry Neurosci (2004); 29(4): 252–65
- Gardner, Adv Psychosom Med (2011); 30: 22–60
- Gresch et al., Neuropsychopharmacology (2005); 30: 1693–1702
- López-Giménez, González-Maeso, Curr Top Behav Neurosci (in press)
- Smith et al., Psychopharmacology (1999); 144(3): 248–54
- Stafford et al., Pharmacol Biochem Behav (2001); 69(1-2):233-7
- Stewart & Baidani, Behav Pharmacol (1993); 4(4): 289-312

LSD is known to activate D2 receptors.

@GerardoFurtado - done

@GerardoFurtado being nicked AliceD I couldn't let this one pass, could I ;-)

@Remi.b thanks for your comments! This question is better asked here than over at Health and in fact is spot on ontopic here imo. This post is all about pharmacodynamics and kinetics, receptor downregulation and neurotransmitter systems. More Bio you possibly can't get, right? But yes, withdrawal effects per se are also on topic at Health, but even more so on CogSci, but then, something being more ontopic elsewhere is no reason to close it here. But again, the question core is neurosci and therefore best asked here. And no, I'm not Alice, my surname starts with an S and I'm a bloke :-)

@AliceD What a deception on your name! I removed my comments and my close vote following you and Gerardo's comments. Thanks


text:
What can cause a lump in the middle of the neck? (homework case study)
What can cause an erythematous, fluctuant, nontender mass in the middle of the neck?
Full Case Study: (Its the last of 6 cases and I just can't figure this one out,  because of all the possibilities, there is always something that doesn't line up.)
The 26-year-old man presented for evaluation of a neck mass and a right axillary mass. The patient, who came to the United States from Vietnam 6 1/2 years ago, noted  midline neck mass. The mass gradually increased in size. Approximately 3 weeks prior to admission, he noted a midline neck mass. These masses were incised and drained twice. Samples of purulent material were sent for routine bacterial culture at an outside hospital. The patient had lost 3 kg (ca. 7 lbs) in the 2 months prior to admission but denied fever. Travel history was notable for his having lived in Arizona for 6 years prior to moving to Boston.
On examination, he was afebrile. An erythematous , fluctuant, nontender mass (8cm x 6cm) was present in the midline of the neck. (Fig. 5.1)  (computed tomogram[CT] scan in fig. 5.2).The right axilla demonstrated incision sites that were draining and were tender to palpation. He had no adenopathy elsewhere. His (PPD) purified protein derivative skin test was reactive, and his chest x-ray was notable for apical scarring in the right lung.
Because of the positive PPD and apical scarring seen on the patient's chest x-ray, the clinical suspicion of cervical ________ was high, and the patient was begun on a four drug anti- _________________ regimen.
Several days after the neck mass was drained of several milliliters of purulent material for culture, a mold was found to grow on the blood agar plates in the routine bacteriology section of the microbiology laboratory. The mold was white (Fig. 5.3) and initially did not have any identifying characteristics when a lactophenol cotton blue preparation was examined under a phase-contrast microscope. It was subcultured at both room temperature and body temperature, and after subculture began to demonstrate the presence of  spores microscopically (Fig. 5.4) The identification was confirmed by using a commercially available genetic probe.

I this a personal medication question?

I've had a case study for a school project, and I've narrowed it down to a fungal infection, I just cant figure out what it is. It grows white on blood agar.

I've voted to close as personal medical/health. Even if it is not "personal" I feel that there is too little information to properly diagnose, and I'm afraid that answers to the question might be misunderstood or misused (as medical advice) by other persons visiting the site.

I would not consider it a personal medication question but more details are necessary to address the question based on general principles. Even the figures that are mentioned in the body of the post are not shown. The final question does not require the case history but the microbiological details are essential, which are missing. Please edit your question accordingly.

You ask for the fungus causing An erythematous , fluctuant, nontender mass (8cm x 6cm) was present in the midline of the neck.
On the brink of question closure I decided to do a quick search. Based on your descriptions, I found a possible culprit.
In the referenced paper they talk about a fungal Cryptococcosis infection causing, and I quote:

[A] fluctuant, non-tender mass, five by five cm. in the right costal vertebral angle which was not red or warm.

So this mass was found on the costal vertebral angle, but the remaining symptoms seem reminiscent of your case study. Fungi generally appear white when plated, as far as I know.
However, more information is likely necessary to confirm this genus and identify the species.

costal vertebral angle (CVA). Source: Pinterest
Reference
- Moore, J Invest Dermatol (1957); 28: 159–82

Why the downvote?

I am not sure who downvoted but I wonder how you could find the answer for a question that does not provide enough details for a reliable microbiological species identification.

@WYSIWYG: I made the answer more reserved.


text:
Why does a human's field of view narrow when moving faster?
A relative of mine is a driving instructor and he regularly likes to bring up that the field of view narrows noticeably when driving at higher speeds.
Is this true, why is this so and does this apply for other species as well (for example, leopards, who are widely known for their fast speed)?

Do you have a citation for this other than the anecdote? I did not notice this effect when looking out of the window in planes and high-speed trains, which travel much faster.

@MarchHo Sorry, I don't have a reference, updated the question. But as per airplanes, no object is actually moving fast in your field of view, as everything is far away.

I mean when looking at the runway moments before takeoff, or a parallel set of rails.

I believe your cousin is referring to what is usually called 'tunnel vision'

stuff on sides of your FOV are moving faster than in the center (right in the center speed is zero, actually). At some speed things on sides will just be a complete blur. Try looking from the window of moving car on hills far away and on the road barrier close to you: same thing for driver

I totally concur with @aandreev - the field of view is a constant (bar any medical issues) and will not change when moving about at any reasonable speed (at the speed of light things might change :-). Attentional focus (subjective percept) may change at high speeds, and physical retinal image slip indeed changes with visual angle as aandreev suggests.

Perhaps it has something to do with adrenalin discharge?


text:
How long do zebra fishes remain transparent?
As larva, zebra fishes are transparent, at least up to 5-6 days. I wonder what would be the upper limit of the transparent period. This is of relevance considering purposes for imaging.
The question primarily relates to normal zebra fish, and not especially to transgenic breeds.

I slightly re-worded your question for clarity. Feel free to roll back.

The upper limit of transparency time of zebrafishes is anywhere from two to three weeks for normal zebrafish for optimal high-resolution imaging. However, there is a modified species of Zebrafish called 'Casper' which is now the preferred zebrafish strain for studies in cancer and other research, because the length of transparency lasts into adulthood.
Sources:

http://medicalphysicsweb.org/cws/article/research/51394
https://biology.mit.edu/people/lisa_steiner#research_summary
http://www.the-scientist.com/?articles.view/articleNo/34834/title/Models-of-Transparency/


text:
Is there a difference between an organizer and inducer substance?
There is a question in my Embryology textbook's exercise that asks about an organizer and inducer substance. I found their definitions and now I am wondering if they are the same things?

According to Merriam-Webster they are synonyms:

[An organizer is]  a region of a developing embryo or a substance produced by such a region that is capable of inducing a specific type of development in undifferentiated tissue —called also inductor

Lifemap and Biology Today support the terms being synonymous as well.
However, I think the most commonly used terminology here is that the organizer [used as a noun] induces [used as a verb] the differentiation of embryonic tissue. For example, consider the following quote (Arizona State University):

The Spemann-Mangold organizer, also known as the Spemann organizer, is
  a cluster of cells in the developing embryo of an amphibian that
  induces development of the central nervous system


text:
Is it possible to merge the genomes of photosynthesizing and electron-transporting bacteria to make an electric cell?
I had an idea of making electric current from bacteria. There are some bacteria that can photosynthesize, and some others are capable of transmitting electrons through each other. Is it possible that through genetic engineering, we could insert the genome that allows bacteria to perform photosynthesis, with other capable of transmitting electricity, and therefor making a bacterial culture, big enough to make a free energy source?

"through genetic engineering" I think this is the kicker. I think you've just described how it would be possible, however actually making it with the current technology would be impossible. Using bacteria to make crude oil is the current best shot at making renewable energy from the sun with biotech as far as I'm aware.

What you're describing is a phototrophic biofilm microbial fuel cell! They're pretty neat.
Essentially the sun powers the bacteria and the bacteria in the anaerobic side passes electrons through the graphite electrode to use oxygen at the cathode. There's another explanation here. You could also "unfold" cyanobacteria and layer them and you'd probably get an efficiency increase but the system would be pretty fragile. Compared to other MFCs, though, everything is fragile. Dirt even works(not very well, but it's dirt).

You do not need to merge anything. Photosynthesis already includes the electron transport across the inner membrane of the chloroplast (in case of plants) or across the bacterial membrane (in case of bacteria), creating voltage difference between inner and outer side. The only problem, this voltage is relatively difficult to take away.


text:
Difference between the inactivation of neurotransmitters and hormones
Neurotransmitters must be somehow removed from the synapse once they’ve produced a post-synaptic potential, whether it be through enzymatic breakdown, diffusion, reuptake or another mechanism. However, I rarely see such mechanisms mentioned when discussing hormonal communication. I assume hormones just diffuse away from their receptor and do not continually stimulate the cell. However, there does not seem to be an urgency in breaking it down. Why is there this urgency, then, in the case of neurotransmitters, but not with other first messengers, like hormones?

I don't quite understand what you're saying. Neurotransmitters and hormones alike are ligands. Dissociation from the receptor is a stochastic process. One ligand can activate a receptor multiple times. Many neurotransmitters are actively removed from the synaptic cleft. What is your question? Why hormones are not removed? Could you limit your question to specific representative example cases?

@AliceD Why are neurotransmitters actively removed but hormones aren’t? Is it not just as imperative to remove the hormone from the binding site?

Does your comment capture the question?

@AliceD I suppose, yes.

I edited the question in response to your comments. If this doesn't reflect your intentions feel free to roll back.

Short answer
Hormones act in the order of minutes or hours. Neurotransmitters in the order of milliseconds. Moreover, hormones are blood-born, neurotransmitters are confined to the synaptic cleft or in the extracelular space directy surrounding the neuron. Hence, their mechanisms of inactivation are different.
Background
The distinguishing feature of hormones and neurotransmitters is the fact that the former are generally released into the blood, while the latter are confined to synapses, or the immediate extracelullar neuronal space. Hence, hormones can be readily cleared by the workhorse of blood clearance: the liver. For example, adrenaline is rapidly (half life 5 - 10 minutes) metabolized mainly by the liver, followed by excretion via the kidneys. Diffusion then will draw adrenaline away from the receptors as blood concentration drops. The relatively slow time course is beneficial, as the effects of epinephrine includes metabolic changes, such as the release of glucose to power up the body (Sherwin & Saccà, 1984). This needs time.
In the synapse, there is no blood flow and inactivation has to occur through other means. Further, epinephrine in the above example is a fast acting hormone. Many hormones work on an even slower time frame. For example, a stress-induced cortisol peak can last for as long as an hour (Kirschbaum & Hellhammer, 2000). Neurotransmitter responses may last for a few milliseconds. For example, some pacemaker neurons may fire at rates of 40-50 Hz (Häusser et al., 2004). Hence, neurotransmitters have to be cleared from the synapse at least within 20 ms. To wait for the released neuroransmitter to passively diffuse out of the synapse is simply too time-consuming. Neurotransmitters act at an entirely different time scale.
References
- Häusser et al., J Neurosci (2004); 24(42): 9215-9
- Kirschbaum & Hellhammer, Encyclopedia of Stress, 3 (2000)
- Sherwin & Saccà, Am J Physiol (1984); 247(2-1): E157-65


text:
Depolarization and hyperpolarization in stereocilia of the inner ear
It’s a well mentioned fact that when the stereocilia of the cochlear hair cells bend in one direction, the hair cell depolarizes, and when the stereocilia bend in the other direction, the cell hyperpolarizes. When the basilar membrane vibrates, the stereocilia are bent back and forth, creating depolarizations in the hair cells followed by hyperpolarizations. What I’m having trouble understanding is why this is significant. This does not determine the frequency of the sound wave, as that is determined by the location along the basilar membrane that the wave impinges on. I don’t see how this would determine amplitude either, seeing as a greater amplitude would only create more drastic bending of a greater number of hair cells. Can anyone shed some light on this?

Great question, and such a pity that the highest quality questions tend to receive the lowest number of upvotes - you have mine!

There are roughly two modes of pitch coding in the cochlea: place-coding and temporal coding. The place-theory is the most prevalent accepted model of how the cochlea realizes pitch coding (e.g., Zwislocki, 1991). Basically, it is based on a frequency-to-place Fourier transformation on the incoming sound, where each frequency is coded on a different place on the basilar membrane, as described accurately in the question.
However, there is another, much overlooked way of coding pitch, namely temporal coding. Up until about 1 kHz, spiral ganglion cells in the auditory nerve and acoustical brain stem regions (such as the inferior colliculus) have been found to respond in a phase-locked pattern (Du et al., 2011). Electrophysiology in auditory nerve fibers illustrates the phase-locked activity in response to low-frequency sounds (Fig. 1). This phase-locking behavior of neurons in the auditory system is called the frequency-following response (FFR).

fig. 1. FFR in auditory nerve fibers. Upper trace shows the stimulus, middle trace a single fiber, and the lower trace the compound activity of many fibers. The group-response faithfully codes the stimulus waveform. Source: New York University.
However, as you rightfully state in your question - why would inhibition of auditory nerve fibers (ANFs) be helpful? Figure 1 illustrates nicely that the auditory nerve FFR is rectified, i.e. only the upper half is coded, while negative action potential counts obviously don't exist; ANFs fire, or they don't, they don't fire negative action potentials. However, one has to realize that a relatively large proportion of ANFs in healthy ears spontaneously fire, i.e., in the absence of sound the auditory nerve is still remarkably active. Spontaneous firing rates vary from 0 to more than 100 spikes/s (Jackson & Carney, 2005). Hence, suppression of spontaneous activity codes pitch too.
Moreover, as a theoretical and un-referenced side note - the auditory system processes acoustic information on the sub-millisecond level. Left/right sound localization is performed by the auditory system by resolving inter-aural time differences (ITDs). By analyzing the delay at which sound arrives in one ear with respect to the other, the localization in the horizontal plane can be estimated. ITDs do not exceed 0.8 ms, given the speed of sound and the size of the human head. This is well below the time it takes for any action potential to develop(!). Hence, by deploying both phases of the sound, one phase being excitatory, the other inhibitory at the ANF level, no time is lost when a sound wave happens to enter the cochlea with its inhibitory flanking phase first.
References
- Du et al., Neurosci Biobehav Rev (2011)
- Jackson & Carney, JARO (2005); 6: 148–59
- Zwislocki, Acta Otolaryngol (1991); 111(2): 256-62

The depolarization and hyperpolarization of stereocilia in the ear is significant for its role in transduction. Hair cells are involved in changing mechanical energy into changes in membrane potential, a process called transduction.
When the cells are displaced and move in the direction of the tallest stereocilium, K+ enters the cell and causes depolarization which allows more transduction channels to open. This depolarization opens voltage gated calcium Ca2+ ion channels. The influx of Ca2+ causes neurotransmitter release from the basal end of the hair cell to the auditory nerve endings which sends signals to the brain.
Movement of the hair cells in the opposite direction causes hyperpolarization which prevents influx of K+ and closes the Ca2+ channels at the base resulting in smaller release, or no release of the transmitter. This allows hair cells to generate a sinusoidal receptor potential in response to a sinusoidal stimulus which preserves the temporal information present in the original signal up to frequencies of 3 kHz.
So the depolarization and hyperpolarization of hair cells is significant because the constant release of transmitter drives the spontaneous activity in the auditory and vestibular nerve fibers. The interaction of Ca2+ influx and Ca2+ dependent K+ efflux lead to electrical resonances that enhance the tuning response properties within the inner ear.
For a more detailed response see: http://www.ncbi.nlm.nih.gov/books/NBK10867/ and http://homepage.psy.utexas.edu/homepage/class/psy394U/hayhoe/perception/Chapt.%201%20Hair%20cells%20of%20the%20cochlea%20copy%203.pdf

So this mechanism codes for frequency?

@lightweaver The mechanism is important because it allows for the conversion of a mechanical sound signal into an electrical nerve signal. Plus the leakage of Ca2+ causes release of neurotransmitter to the synapse which allows hair cells to respond quickly to mechanical stimuli.

This does not answer the question. Albeit accurate, it's not more than an overview of how mechanoreceptors work in general.


text:
Why Doesn’t Hypercalcemia Cause Muscle Spasms?
If you have more calcium in the cell, wouldn’t more attach to troponin and initiate muscle contraction? Why does hypercalcemia cause muscle weakness instead of spasms?

Muscle weakness caused by hypercalcemia might come from a decrease in excitability (so that less contractions are initiated) rather than from the contraction mechanism itself.

Hypercalcemia does indeed cause muscle spasm, but as someone else wrote, hypercalcemia indicates the calcium levels in blood and not in the sarcoplasmic reticuli.
One example where you can observe that increased calcium leads to increased contraction is when you take the cardiac glycoside, digoxin. Digoxin inhibits the Na+/K+ ATPase causing an increased concentration of intracellular sodium ions. Indirectly, the increased levels of sodium will disturb the sodium gradient (because of the accumulation of sodium ions inside the cell) and stop the Na+/Ca2+ exchanger. The consequence of the disturbance of the sodium/calcium exchanger will lead to the increased levels of calcium and the increased storage of calcium in the sarcoplasmic reticulum and thus cause positive inotropy of the myocytes.
You can read more about it here:
Gheorghiade, Mihai, Kirkwood F. Adams, and Wilson S. Colucci. "Digoxin in the management of cardiovascular disorders." Circulation 109.24 (2004): 2959-2964.

Can you please provide a textbook/paper reference for your statements?

Look under "Mechanism of Action" here : http://circ.ahajournals.org/content/109/24/2959.full

Lets think about sodium channels for a moment. Empirical studies show that calcium has the ability to transiently block sodium channels (1). So if you have a high amount of calcium floating around, what you're doing is blocking the flux of sodium through the neural membranes. Neurons aren't going to fire if there's little or no flux through these sodium ion channels, so if the neurons decrease in their firing rate, yo end up with muscle weakness.


text:
Are more molecules of ADP than inorganic phosphate returned to the light reaction in photosynthesis?
During the dark reaction, 9 molecules of ATP are consumed for every 3 carbon dioxide molecules, yet only 6 molecules of inorganic phosphate ultimately leave the cycle. Does that mean that there is a greater concentration of ADP than inorganic phosphate returning to the light reactions?

Not 6, but 9 molecules of Pi are formed in the Calvin cycle, from the conversion of 9 ATP to 9 ADP:

Source: Columbia University

I thought the inorganic phosphates were incorporated into phosphoglycerate to form DIphosphoglycerate, but then given off again in the formation of G3P. Then it is once again incorporated into glyceraldehyde phosphate to form ribulose BIsphosphate, but is not released anywhere else.

There's definitely some confusion. In the C3 cycle reactions, the conversion of 3-phospho-D-glycerate to diphosphoglycerate (DPG) actually affixes the inorganic phosphate from ATP to the DPG. The reaction that follows releases NADP+ and inorganic phosphate at a ratio of 2 per CO2 in the cycle, so for 3CO2 used in making one half a glucose, thats 6 inorganic phosphate liberated. If you're also considering the regeneration of rubisco, two inorganic phopsphate are liberated there for a total of 8 inorganic phosphate in the products per 3CO2.

And then, here's a link to a more detailed reaction schematic:
http://www.chem.qmul.ac.uk/iubmb/enzyme/reaction/polysacc/polygif/Calvin1.gif


text:
Photolysis of Water?
In chemistry, I studied the decomposition of water as being $2H_2O_{(l)} \rightarrow 2H_{2(g)} + O_{2(g)}$. However, when water is split, the equation is $2H_2O_{(l)} \rightarrow 4H^+ + 4e^- +O_{2(g)}$. Why is that? How does $H_2$ just ionize?
Moreover, what is the mechanism for photolysis? I would have thought that splitting water molecules requires a ton of energy; yet it can be accomplished simply with light energy during photosynthesis?

Have you read about the photosynthesis in detail? I think this will explain the question.

I don't want to write the same again: http://biology.stackexchange.com/a/23829/3703 use this and read about redox reactions.

The part of photosynthesis occurs in the granum region of thylakoid region of a chloroplast when light use absorbed by chlorophyll. It is the break down of water molecule into hydrogen and oxygen under Influence of light when photons are absorbed, it causes the hydrogen to bind to an acceptor, subsequently releasing oxygen.

Water is split in chloroplasts in the light reaction of photosynthesis. Chlorophyll, acting as a photopigment, captures sunlight and transfers that energy to an electron pair of a water molecule. Under the influence of a water-splitting enzyme (George et al, 1989) it is separated into 2 protons, molecular oxygen and a free electron pair.
Reference
George et al. Science 1989; 243(4892): 789-91

The splitting of water in chloroplasts is catalysed by the Oxygen Evolving Complex. It's all about redox reactions but in general hydrogen is the less electronegative of biological elements so it is easily ionised in many life reactions.


text:
All-trans-retinal being converted back to 11-cis-retinal or vitamin A
There are two pathways all-trans-retinal can take after detaching from the scotopsin: (1) it can convert back to 11-cis-retinal, or (2) it can convert to all-trans-retinol (form of vitamin A), which then converts to 11-cis-retinol and then 11-cis-retinal. My question is what factors determine which pathway will occur?
The first sounds like it doesn’t involve vitamin A at all and just recycles the retinal. Hence it wouldn’t be affected by any vitamin A deficiency, yet we know vitamin A deficiency affects the stock of retinal in the eye. Yet I don’t see any disadvantages in simply recycling our retinal; why would we go through the process of converting it to vitamin A and then back to 11-cis-retinal?

Short answer
A complex visual cycle in vertebrates involving vitamin A is useful for storage, re-distribution of retinoids to both rods and cones, to improve photosensitivity and reduce noise in the visual system.
Background
The visual cycle in mammalian rods is depicted in Fig. 1.

Fig. 1. Visual rod cycle. Source: Palczewski (2010)
11-cis-retinal isomerizes to all-trans retinal by absorption of a photon.  Your notion that this pathway can involve direct re-isomerization back to 11-cis-retinal is only true for invertebrates. They simply absorb another photon to back-isomerize all-trans to 11-cis (Saari, 2012).
In vertebrates, however, this bi-stable configuration is replaced by a complex visual cycle (or retinoid cycle, Fig. 1). The reason is that the bi-stable invertebrate system is less sensitive, as photons used for regeneration cannot be used to initiate phototransduction. Moreover, the invertebrate system is more prone to noise, as photons can both start the phototransduction or recycle all-trans retinal (Saari, 2012).
In vertebrates it is thought that the visual cycle only emerged after appearance of the cone system (Saari, 2012). Notably, the visual cycle depends on the retinal pigment epithelum (RPE), as shown if Fig.2.

Fig. 2. Rod and cone visual cycle. Source: Saari (2012)
Fig. 2 shows that vitamin A (all-trans-retinol) is present in the RPE. RPE cells are able to store vitamin A by converting it to fatty acids and store it in oil droplets. Moreover, RPE cells can funnel this stored vitamin A to both rods and cones, another reason why the complex visual cycle and vitamin A conversion makes sense (Palczewski, 2010)
References
- Palczewski Trends Pharmacol Sci (2010); 31(6): 284-95
- Saari, Annu Rev Nutr (2012); 32: 125–45

It's entirely wrong statement about sensitivity. Invertebrate photoreceptors are extremely sensitive compare to vertebrates and they can respond to ideally single photon (Randall et al 2015, Hardie 2001 )

@Dexter - one photon is necessary to regenerate invertebrate photopigment after absorption of the first photon. Efficiency=sensitivity hence reduced by 50%. Vertebrate rods can too respond to a single photon.

You might want to look at this. I remember one review comparing sensitivity of both. I am looking into it. And I don't think "efficiency=sensitivity" is true.

@Dexter the responsiveness of photoreceptors also depends on their stack number, height, concentration of photopigment and what not. The simple fact is that when you use x to convert A to B and x to recycle B to A, it's noisy and inefficient. And using two photons to detect one is per definition less sensitive than detecting one and independently recycling the pigment.

I think it's better to provide reference for claim than fight over different points. Another logical points I can raise is that Calcium channels are being closed in vertebrates in contrast to invertebrates. And opening of channel (which also has strong calcium feedback) is much faster than closing channels (which also has calcium feedback but on 100x slower time scale).

@Dexter - references are provided and I am not fighting. And I have never ever said the vertebrate system is fast. Don't put words in my mouth.

Let us continue this discussion in chat.


text:
Understanding the "Waterfall Illusion"
Motion after-effect illusions, such as the waterfall illusion, refer to illusions where fixating a screen which shows stimuli moving in a particular direction  elicits the perception of motion in the opposed direction when subsequently looking at a static image.
Here is an example: Video Motion After-Effect
The explanation is typically that adaptation effects lead to a saturation of the firing rates of neurons encoding the viewed motion direction.
So far so good - but why do we then perceive afterwards motion in the opposite direction, and not in any other direction where no adaptation has happened?

This is a more detailed answer about conceptual mechanisms from the same author as AliceD is citing:
The first row represents the sensors (for instance photoreceptors) while the second row
represents higher order responses (for instance of MT neurons). The latter's response is their resting level response plus the difference of the corresponding channel minus the opponent channel's response (so yes, the assumption is that there is an opponent mechanism). As you can see, there is no response beyond baseline before adaptation
as the difference between the sensor's responses is zero. During adaptation, when subjects are seeing an upward motion, the corresponding response is higher, too.

Now after adaptation, the opposed system shows an above baseline response as now the up sensors display some form of adaptation, hence shifting the response difference of the sensors in the favour of the opponent motion direction:

I am not familiar with the underlying biophysical mechanisms, this model possibly suggests, however, decreased feedforward inhibition after adaptation.
Mather, the motion aftereffect: a modern perspective

The motion after-effect (MAE) is believed to be primarily due to adaptation of direction sensitive cells in the middle temporal area (MT) (Fig. 1.). The directional cells in this area of the cortex are selectively sensitive to motion in one direction. Hence, looking at a waterfall will selectively cause adaptation in those cells tuned to the direction of the waterfall. When one looks away, the MT cells responsive to opposite directions will become dominant, as their counterparts are momentarily shut down and one will see the waterfall running in opposite direction.
Adaptation thus apparently weakens the opponent input to the adapted MT cells, enabling an enhanced response to motion balanced stimuli. However, the possibility of adaptation occurring in MT neurons themselves cannot be ruled out (Mather et al., 2008).
The MT area is one of the principal visual cortical areas devoted to motion sensing and hence a likely culprit for MAE. However, fMRI studies have indicated that a lot more visual areas in the brain may be involved, either directly, or indirectly, including V1, V2, V3, VP, V3A, V4, and also MT (Mather et al., 2008).

Fig. 1. Two visual streams dominate vision: the dorsal 'where" pathway (containing the direction-sensitive MT area), and the ventral 'what' pathway. source: InTech Open
Reference
- Mather et al., Trends Cog Sci (2008); 12(12): 481-7

Ok thanks, but my question is not so much about the where (I am somewhat aware of MT and the dorsal stream, and that the size of the adapted area allows us to infer if it is a upstream inferred property or happens in MT itself), but why it is exactly the 180 degree opposite direction which then becomes perceptually salient, and not say the direction which is 32 degrees different. I am not sure if your answer addresses my question

@user234 the MT cells are sensitive to specific directions, per the answer, so yeah, I'm covering the Q pretty heads on I guess

Ok but then I just don't get it from your answer, and would like to understand better: I get that the cells are selective, ie tuned, for a particular motion direction. But when firing rate to this motion direction is attenuated, why is it exactly the opponent direction which becomes perceptually salient? What's the mechanism? Like there must be some opponency mechanism for directions different by 180 degrees I guess?


text:
How does slowed action potential propagation in the optic nerve cause blurred vision?
Multiple sclerosis is accompanied by optic neuritis, and there is demyelination of the optic nerve, causing the action potential to be propagated more slowly along axons. But how does this lead to blurred vision?

Demyelination per se is not the whole story behind the blurring of vision seen in MS patients.
MS results in an inflammation of the optic nerve (optic neuritis) and demyelination of the optic nerve fibers. It is commonly seen in MS, and is associated with blurred vision, basically because the signals are not sent properly along the optic nerve. Blurred vision in MS can have several reasons. These include:

On the one hand blurring of vision is caused by the swelling and loss of optic nerve fibers due to the inflammatory effects accompanying optic neuritis.
The demyelination of the optic nerve fibers associated with optic neuritis caused by MS disrupts signal transmission especially in the central eye field, leading to blurry parts in the center of focus due to impaired neurotransmission.
Another symptom of MS is double vision, this is caused by demyelination of neurons in the brainstem that coordinate the control of the muscles that control eye movement. If the eye muscles are not working properly, and especially if one side of the brain is affected more than the other, it will cause blurred vision, because both eyes do not move in a synchronized fashion anymore.


text:
How did bullying arise evolutionarily?
By bullying, I mean individuals harassing others with name-calling or violence but not for the purpose of gaining resources such as with extortion or theft. The only explanation I've thought of is that bullying offers practice for types of extortion that do result in increased resources.

What you might find interesting is now many domains of study can contribute to your answer. For example economics and culture might play a part in the onset of behaviors deemed oppressive or intimidating.

Having an ennemi is the best way to have friends. bullying is a group activity and would possibly be performed so to increase the level of trust within a group of friends.

@AliceD please never ever suggest cross-posting. We try very hard to avoid duplicating questions on multiple SE sites. If a question can fit on both sites, it should be tweaked to ask for different aspects of the issue based on each site's scope, not repeated.

Asking for examples of bullying in species other than humans, and reasons/context for these behaviours will probably be more fruitful and easier to answer. This can hint at the evolutionary context for bullying in humans as well. Evolutionary “how” questions are usually extremely hard to answer.

@fileunderwater Well, the OP did mention namecalling, which implies interest in the evolution of human bullying. So a "human-centric" answer seems appropriate. Also bear in mind that any given trait can provide multiple benefits, and as such can arise for different reasons in different situations. Basically, bullying may have evolved in our species for slightly different reasons compared to why it did so in other species. Convergent evolution may favor bullying for many reasons, and so focusing on human bullying again, would not seem inappropriate.

I think bullying is really more of an emergent behavior that manifests itself because of natural aggression built in for survival, as well as our complex social-based psychology leading to insecurity when dealing with other:

People who are highly aggressive, and or apathetic to the suffering of others are more likely to control a majority of resources if they don't face significant opposition. This leads to their favored propagation obviously. Then, in their free-time, with all resources under control, they simply continue to do what comes naturally to them: dominating others. It can also work even in those without the ability to actually control resources, due to lack of intelligence for instance. I have met far more non-intelligent bullies than the reverse. The reason for their behavior is still explained by an attempt to control their territory and social status, however ineffective.
Again, due to our complex psychology centered around social interaction, we can develop insecurities about our self-perceived 'fitness', and therefore acceptance by mates and peers. This low self-esteem can lead to bullying others to boost one's ego. Chemically, this can result in a release of endorphins because they feel they have achieved something, which supports bullying behavior as an emergent behavior. Also, those with lower intelligence are likely to have trouble with reasoning skills, and therefore find it difficult to self-analyze and realize their behavior is negative. This leads to bad interactions with others, which can make those individuals feel even more insecure, which in turn fuels their drive to assert themselves through bullying.

Many studies have been conducted on sociopaths/psychopaths. Just like any other evolved trait, whether or not their "personality disorder" is beneficial to the propagation of their genes depends on environmental factors. If they face only opposition from entities that are relatively weak, physically and mentally, then they have an advantage over those peers. But if their peers are sufficiently strong and organized, then the personality disorder becomes a disadvantage if they can't adapt, because they will be attacked by those seeking cooperation from others when they misbehave. Obviously, when our species' numbers were few, high-aggression and a willingness to kill for resources needed for survival aided in survival. In these modern times, its less acceptable for socio/psychopaths to display their innate behavior, due to modern laws, but obviously society can take turns that allow them to express themselves without worry...see the holocaust or any other genocide for an example.
https://link.springer.com/article/10.1007/s40806-017-0097-5
https://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=2&cad=rja&uact=8&ved=2ahUKEwj5vKjk88bjAhUfJTQIHaFDA9wQFjABegQIARAC&url=https%3A%2F%2Fwww.apa.org%2Fpubs%2Fjournals%2Freleases%2Famp-a0038929.pdf&usg=AOvVaw1fUJiPHl8rSKMm6Gc9VEeA

Can you provide some references.

While I do not have references of studies on this exact focus, I will post references tomorrow concerning the genetic propagation of genes leading to aggression, as well as references concerning the link between aggressive social behavior and genes, with aggression serving as a means of increasing genetic propagation.

Next time onwards please try to include references for your answers. Also feel free to use help centre for any assistance that you need in order to create a proper answer or a question. Your answer may be down voted if you are not providing any references for them, and it will affect your reputation(if you cares). :)

It is extremely hard to prove a negative.

I find this answer very human-centric and it seems to be framing bullying a priori as “bad”. See e.g. statements on social insecurity and sociopaths. Given how common bullying is in human societies, across time, in different contexts and levels, I don’t think that is the most fruitful way to speculate on the evolutionary background. I doubt that bullying should be seen as an unfortunate side-effect, given how common similar behaviours are in other group-living/social animals, from apes to wolves and birds (e.g. poultry).


text:
Evolution of Chromosome Numbers
Some species have different numbers of chromosomes, as we all know. Throughout evolution, how was a species able to survive with an extra chromosome? How was this organism able to breed successfully to form offspring with the additional chromosome?

+1 good question. I guess that an added chromosome probably come from the duplication of another chromosome yielding to a partial polyploidy. Under this assumption it might be interested to look at the work of Sally Otto on change in ploidy number. I think we might intuitively overconsider the importance of such duplication on the functioning and health of the cell. I would tend to think that the big issue has to do with dosage compensation (amplitude of gene expression). Also, such duplications have the advantage to hide recessive deleterious allele.

possible duplicate of Evolutionally speaking, why do humans have 46 chromosomes

I don't think those should be considered duplicates. On the other hand, I seem to remember another very similar question. Does anyone know it?

possible duplicate of How are new chromosomes replicated into the next generation via sexual reproduction?

Chromosome splits (or fusions for that matter) might not mean that much for reproductive success since genes can still line up and recombine. To quote the science blogger P.Z. Myers:

[C]hromosome numbers can change dramatically with no obvious effect
  on the phenotype of the organism.

He illustrates it thusly:

So to answer your first question, changes in the number of chromosomes aren't always fatally deleterious (as you seem to think).
As for how a change in chromosome number might spread, the explanation is likely random drift and inbreeding. To quote P.Z. Myers again:

So our two chromosome individual will have a reduced fertility as long
  as he or she is breeding with the normal one chromosome organisms, but
  those split chromosomes can continue to spread through the population.
  They are not certain to spread — they’re more likely to eventually go
  extinct — but by chance alone there can be continued propagation of
  the two chromosome variant.

"Evolution" by Mark Ridley, p. 361 similarly points out that reproduction will be an uphill battle until the new variant becomes more common (often through inbreeding or drift in small populations):

When a new chromosomal fusion mutation arises, it will be selected
  against because of its disadvantage in heterozygous form. But if it
  drifts up to a locally high frequency, as may easily happen in a
  local, small, and perhaps inbreeding, mouse population, natural
  selection will favor it. Natural selection favors whichever
  chromosomal form is locally common[.]

This might in the end lead to speciation due to the two populations becoming incompatible.

What about the very first organism to get an extra chromosome? Assuming it was a very small organism, wouldn't the need to replicate an extra set of chromosomes be very resource demanding to the organism and therefore possibly cause death? Or was this effect not very significant on the organism's chance of survival?


text:
Can you build muscles from watching point of view videos of people weightlifting?
According to this, "new research has found that viewing other people exercise actually increases your heart rate and other physiological measures, just as if you were working out yourself".
This got me thinking, can muscles be developed to be stronger and bigger from simply watching videos of people weightlifting from the point of view of the weightlifter?

This post might interest you.

You could always post this on Skeptics, although I like anongoodnurse's answer here.

That is highly unlikely.
The article to which you linked specifically states:

While watching other people exercise may increase your heart rate and have other physiological effects, nothing can replace the health benefits of getting off the couch.

With proper nutrition, muscle is built through exercise by

adding sarcomeres [to muscle cells which is] physiologically determined by the degree of force a muscle can generate that is in turn dependent on the degree of overlap of the thick and thin filaments. Thus, the amount of tension would control the number of in-series sarcomeres in a single muscle fiber.[1]

Watching a show about cooking might stimulate hunger, but it won't put food into your stomach. Watching something that evokes a sympathetic response (fear, fighting, an attractive person exercising vigorously, an athlete in a competitive event, etc.) will elevate heart rate, sweat production, and resting muscle tension, but there is not enough tension to produce muscle growth.
In addition, there might be small deleterious effects to watching emotionally charged movies which elicit a sympathetic response: they cause stress. An effective horror film will elicit tension and maybe even a startle response - making you jump in your seat - but it will also elevate your blood pressure, etc.
Exercise is good for you physiologically. Simple stress without exercise is much less so.[2]
[1] Muscle growth and exercise
[2] The Physiology of Stress: Cortisol and the Hypothalamic-Pituitary-Adrenal Axis (simplified but relevant)

I doubt it. Muscle growth comes from literally damaging muscle fibres by putting them under too much load. This is what causes the muscle pain after a workout. This triggers thickening and increase in number. Without the damage in the first place, there's no reason for the fibres to change.


text:
identification of species of tree
I just want to confirm the species of the tree in the middle of the picture. Is it the "Flame of the Forest"? This is taken in my school campus. Thanks in advance!

I would be good to be able to see the leaves in detail. This makes an identification easier.

This question appears to be off-topic because it is about plant identification. These questions are usually asked on Gardening and Landscaping Stack Exchange.  This topic is not found in the following appropriate topics listing in the Help center:                          1) General questions about biological concepts
2) Questions about the biological mechanisms behind medical conditions
3) Questions about techniques in a biological or biochemical laboratory

It looks like a Royal Poinciana tree with the scientific name Delonix regia..

Please refer to this link for more info


text:
Differences Between Protein Motifs and Protein Domains?
I am in a 300-level molecular biology class and am unclear about this concept and how to delineate motifs versus domains of proteins.  Any suggestions would be much obliged.

These are completely different concepts, which sometimes may be connected.
A motif in biology is a mathematical model, typically of a sequence, that predicts which sequences belong to some defined group. For example, a DNA sequence motif can characterize the binding site of a transcription factor, i.e. which sequences tend to be bound by this factor. For proteins, sequence motifs can characterize which proteins (protein sequences) belong to a given protein family. A simple motif could be, for example, some pattern which is strictly shared by all members of the group, e.g. WTRXEKXXY (where X stands for any amino acid). There are also more complex motif models.
Protein domains, on the other hand, are a structural entity, usually meaning a part of the protein structure which folds and functions independently. So, proteins are often constructed from different combinations of these domains.
So how are motifs and domains related? Well, when you think about protein families, it makes sense not only to look at the whole sequence but also to focus on individual domains. Since they are a elementary functional-structural units, it makes sense to find sequence motifs for individual domains. So, you often find that a protein contains multiple domains, each domain characterized by having a sequence that matches the motif of its family.

adding to the answer of @Bitwise:
Motif is just a statistically well represented pattern in a data. It can be a sequence or even a structure. Motifs CAN be sometimes associated with particular functions

@WYSIWYG thanks for the clarification, I was going to mention structural motifs but forgot to write it.

This was very helpful, thanks for the reply. :)

The principal difference is that domains are independently stable, while motifs are not.
Here is a bit on motifs: http://www.sinauer.com/pdf/nsp-protein-1-16.pdf
A motif can be part of a domain.  From there:

The second, equally common, use of the term motif refers to a set of
  contiguous secondary structure elements that either have a particular
  functional significance or define a portion of an independently folded
  domain.

Expanding on the comment made by @WYSIWYG, a motif is just a pattern. For proteins this pattern can either refer to a string of amino acids — a sequence motif — or the conformation and interaction of residues in space — a three-dimensional structural motif.
It is important to qualify the term ‘motif’ to indicate precisely what is meant.
Sequence motifs
A good illustration is the ATP-binding motif:

GXXGXFKS(or T)

This illustrates that not all positions need be specified (X) and that in some positions alternatives may occur (S or T).
Structural motifs
One type of structural motif involves small hydrogen-bonded structures such as beta-bulges, Schellman loops and beta-turns. A beta-turn is illustrated:

It can be simply defined as “A motif of four consecutive residues and one H-bond in which a H-bond occurs between main-chain CO of residue-1 and main-chain NH of residue-4”. Alternatively, subcategories can be defined in terms of the dihedral angles at residues 2 and 3.

After the peptide chain of a protein has been organised into successive stretches of secondary elements, combinations of such elements are first arranged into distinctive groups called super secondary motifs. Several neighbouring secondary elements and supersecondary motifs are folded and twisted further into compact globular cluster called a domain.


text:
What is the difference between different brain regions
The brain is separated into different regions, and different regions perform different tasks. Well, what are the differences between these regions on the cellular/systemic level. The brain is made up of neurons and other cells, but how come one part is used to process sound and another is used to process, say, smell? Are they like different computer circuit boards - using the same components but are wired differently?
And anyways, why did evolution not come up with a brain that uses the entire brain to process something, would that not be more efficient?

The wiring is different as you mentioned. However, perhaps the most important is the brain knows where it's input is coming from. The brain knows where each fibre innervates and thus can compile and present this data to our conscious mind. We show if we stimulate the brain directly, than we feel a sensation in the part of the body that portion of the brain is responsible for. Plasticity means our brain can change what feeds into where, this is most commonly where we learn a motor skill. If we play the piano for example the part of the cortex feeding to this area increases.
Another way is the type of chemical transmitter and receptor. Dopamine is primarily used for things that cause us pleasure for example. However dopamine can affect our movement if it is secreted in from the substantia nigra, as this feeds into the motor cortex. Furthermore, neurotransmitters can be excitatory or inhibitory and this is an analogue rather than binary signal. All of these fine tune, and the position at which they inhibit and the location and the feedback from which they obtain their signal all indicates from where the brain is getting the information or to what it is responding to.
In summary it is wiring, signalling and location. However the components are incredibly similar but it isn't the small differences that have a profound effect.

OK, thanks for your answer, but WHY is this more efficient that if they are not separated? Why can't every part of the brain (at least the cortex) perform every function? Or can it? If a part of someone's brain is missing, would the other parts eventually be wired differently to 'replace' the missing part?

You have a machine that makes ice cream, a machine that makes bread and a machine that makes cookies. You lose the machine that makes cookies, would you use the ice cream maker or the bread maker? Would they be as good? That's how it works. Parts of our brain are specialised because they adapt as we use them. If we lose one part another part can take over that typically can mimic some of the function, but it isn't as great. If the part is unique then our brain has more difficulty. However it will unlikely be as efficient unless we train it to high degrees. That's a general theory.

If it wasn't clear why this means we have different regions catering for different things, then it is about efficiency. Using specialised well-adapted equipment is much better than using general stuff for everything.

It may be important to point out that different sensations (touch, smell, sight etc) are encoded by means of the same machinery (e.g. neurons, glia) using the same code (e.g. action potentials, calcium waves). If we stimulate a subject's visual cortex using an electrode he will experience visual sensations, although he would not be seeing real things.

The brain is separated into different regions, and different regions perform different tasks

Not really. This kind of claims stem from the early brain research, where every area was thought to specialize in one particular task. Sure, some categorization is possible (e.g. where the visual input is mostly processed). However, your question is basically an argument that is false.
Just look for example the temporal lobes and compare how the sulcal and gyral areas differ with respect to information processing.

We don't know yet in detail how different cortical areas are wired up, so it's difficult to say to what extent the wiring differs. But the overall structure of different cortical areas is remarkably similar, in terms of the layers of cortex and their cellular components.
Certainly the structure of the input is very different between cortical areas, and cortex seems to take great care during development how that input is structured.
We don't know why cortex is parcellated the way it is. But connections within cortical areas devoted to a single "function" are much more prevalent than connections between cortical areas. This suggests two things: many connections are required between neurons processing similar information, which implies that those neurons should be close together, because wire is expensive in the brain (i.e. requires resources and takes up a lot of space); alternatively, maybe the information is easier to process if it's kept physically separated.