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Pie Chart Activity
A Pie Chart activity differentiated 3 ways. Including some 2 steps problems.
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Four booklets over 36 pages covering transformations (excluding negative and fractional scale factors). A second copy of these booklets containing answers is also included. The booklets cover doing and describing, of course, and they really allow learners to build their skills from a very basic level. All work can be completed in the booklets.
Benin Planning and Resource Pack KS2
Benin AD 900-1300 is now a non-European study unit for KS2 on the new curriculum for history.
 This ten-lesson history unit contains lesson plans, pupil resources and teachers' guides.
 Everything you need to teach this unit.

 This unit covers the following questions:

 1. What was the Kingdom of Benin?
 2. How was the Kingdom of Benin first established?
 3. What did the people of Benin Kingdom believe?
 4. Why did the first dynasty of Ogiso come to an end in AD 1180?
 5. What were the Obas like as leaders?
 6. What did ordinary people do for jobs in the Kingdom of Benin?
 7. What was Benin Kingdom art like?
 8. What happened to Benin Kingdom after the period AD 900-1300?
 9. What was left after Benin Kingdom was destroyed?
 10. What have we learned about this period of history?

 All the plans and resources are produced by Ofsted-rated outstanding teachers.
By KS2History
GCSE Foundation Maths Complete Revision AQA Edexcel
A GCSE Foundation Maths PowerPoint presentation I created from some revision worksheets I use. It contains slides on how to answer all the types of questions that may come up in the foundation exam. It was created with AQA and Edexcel (foundation) in mind, but may be suitable for other exam boards too.

 Additionally, could be good revision for Higher GCSE students too. I use it with my high KS3 Students as they are more than capable understanding the material.

 I have split it up into four areas: Number, Algebra, Data/statistics, and Shape/Space/Measures.

 All funds raised by the sale of this resource will be donated to the NSPCC.

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GCSE Maths KS4 specifications for 2015 in Word
An extremely useful resource that has almost unlimited application.
 I've taken the GCSE Maths specifications for 2015 and converted them into MS Word tables, landscape and portrait, mostly fitting on to one side for each area - number, algebra, etc.
 They can be used for planning lessons, schemes of work, cutting and pasting into lesson aims and objectives, or for recording pupil/learner achievement on each objective.
 In Word they are very adaptable, and columns can be added as required, for dates etc.
By colinbillett
Solar Eclipse Fact sheet
A few answered questions about the up and coming solar eclipse on Friday 20th march.

 All text and images have been put together by me.
 The images of the Sun, Earth and Moon are not to scale.
 The angle of tilt of the Moon's orbital path is drawn to illustrate the point not accurate to the real movement.
 The answers to the questions are my interpretations of fact learnt over the years and cannot therefore be sourced. I am a qualified Physics teacher with 17 years experience of teaching.
By MrsHeelam
Factorising Quadratics Lesson(s)
This a complete set of lessons on factorising quadratic expressions.
 Starter includes expanding single and double brackets, all answers included
 Then, a nice 'Products and Sums' task where students, on mini whiteboards, find which numbers have a product of ... and a sum of... .
 LOs, before examples for you to cover with your class on each permutation of signs in the brackets once factorised - a very scaffolded approach to suit lower ability students.
 All answers included for questions posed to students.
 Other starter activity is to find pairs of expressions that match before continuing with the series of lessons.
 Finally, a 'My favourite No' (see my blog mrcollinsmaths.blogspot.co.uk) plenary task to review students learning.
By paulcollins
Transformations KS4 - presentations, puzzles, worksheets and more
A full set of resources for developing transformations at KS4 or build upon my other resource at KS3. An introduction of the four transformations of KS3, or review of symmetry, which can be done by children on an interactive board. Then a full presentation of the four at KS4 with rotations, reflections, translations and enlargements, with lots for the learners to try. Plus a worksheet with eight questions from GCSE to complete. A multiple choice quiz for plenary or recap in the next lesson. A full lesson plan is included, plus objectives. An exciting lesson that reviews and builds upon existing knowledge. All images ©2015 Colin Billett
By colinbillett
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Roles for Pituitary Adenylate Cyclase-Activating Peptide (PACAP) Expression and Signaling in the Bed Nucleus of the Stria Terminalis (BNST) in Mediating the Behavioral Consequences of Chronic Stress
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DOI: 10.1007/s12031-010-9364-7
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- Hammack, S.E., Roman, C.W., Lezak, K.R. et al. J Mol Neurosci (2010) 42: 327. doi:10.1007/s12031-010-9364-7
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Anxiety disorders are frequently long-lasting and debilitating for more than 40 million American adults. Although stressor exposure plays an important role in the etiology of some anxiety disorders, the mechanisms by which exposure to stressful stimuli alters central circuits that mediate anxiety-like emotional behavior are still unknown. Substantial evidence has implicated regions of the central extended amygdala, including the bed nucleus of the stria terminalis (BNST) and the central nucleus of the amygdala as critical structures mediating fear- and anxiety-like behavior in both humans and animals. These areas organize coordinated fear- and anxiety-like behavioral responses as well as peripheral stress responding to threats via direct and indirect projections to the paraventricular nucleus of the hypothalamus and brainstem regions (Walker et al. Eur J Pharmacol 463:199–216, 2003, Prog Neuropsychopharmacol Biol Psychiatry 33(8):1291–1308, 2009; Ulrich-Lai and Herman Nat Rev Neurosci 10:397–409, 2009). In particular, the BNST has been argued to mediate these central and peripheral responses when the perceived threat is of long duration (Waddell et al. Behav Neurosci 120:324–336, 2006) and/or when the anxiety-like response is sustained (Walker and Davis Brain Struct Funct 213:29–42, 2008); hence, the BNST may mediate pathological anxiety-like states that result from exposure to chronic stress. Indeed, chronic stress paradigms result in enhanced BNST neuroplasticity that has been associated with pathological anxiety-like states (Vyas et al. Brain Res 965:290–294, 2003; Pego et al. Eur J Neurosci 27:1503–1516, 2008). Here we review evidence that suggests that pituitary adenylate cyclase-activating polypeptide (PACAP) and corticotropin-releasing hormone (CRH) work together to modulate BNST function and increase anxiety-like behavior. Moreover, we have shown that BNST PACAP as well as its cognate PAC1 receptor is substantially upregulated following chronic stress, particularly in the BNST oval nucleus where PACAP-containing neurons closely interact with CRH-containing neurons (Kozicz et al. Brain Res 767:109–119, 1997; Hammack et al. Psychoneuroendocrinology 34:833–843, 2009). We describe how interactions between PACAP and CRH in the BNST may mediate stress-associated behaviors, including anorexia and anxiety-like behavior. These studies have the potential to define specific mechanisms underlying anxiety disorders, and may provide important therapeutic strategies for stress and anxiety management.
KeywordsPituitary adenylate cyclase-activating polypeptide (PACAP)Corticotropin-releasing hormone (CRH)Bed nucleus of the stria terminalis (BNST)AmygdalaChronic stress
The Bed Nucleus of the Stria Terminalis
The BNST is a complex brain region and has historically been divided into anterior and posterior regions by the fibers of the stria terminalis, and further divided into medial and lateral subdivisions (Ju and Swanson 1989; Ju et al. 1989). Swanson and colleagues have defined as many as 30 subdivisions based on cytoarchitecture, chemoarchitecture, and connectivity (Dong et al. 2001b). However, one anterolateral BNST region of particular note is the oval nucleus (Fig. 2); the oval nucleus is activated by stressors, demonstrates high levels of pituitary adenylate cyclase-activating polypeptides (PACAP) and CRH expression, and is associated with affective behavior (Kozicz et al. 1997; Day et al. 1999; Walker et al. 2003; Funk et al. 2006).
The BNST and peripheral stress responding
As discussed above, threats to homeostasis activate many CNS-coordinated stress responses (Fig. 1). The neuroendocrine stress response is initiated by increased hypothalamic PVN CRH biosynthesis and secretion into the pituitary portal system, which in turn elicits the release of anterior pituitary gland adrenocorticotropic hormone (ACTH) and downstream release of glucocorticoids from the adrenal cortex. Hypothalamic CRH neurons also regulate the autonomic stress response via fiber projections to brainstem and lower spinal nuclei (Arborelius et al. 1999; Ulrich-Lai and Herman 2009); the activation of catecholaminergic sympathetic fibers results in the peripheral release of these catabolic neurotransmitters. The measurement of plasma glucocorticoid and catecholamine levels as end-points has long been used to confirm the stressful nature of experimental manipulations. Critically, CRH signaling from the PVN appears to be a central regulator of both the endocrine and autonomic pathways which provide the organism with coping strategies in the face of homeostatic threats (Herman and Cullinan 1997; Ulrich-Lai and Herman 2009).
Depending on the nature of the stressor, the hypothalamic PVN, in turn, can be driven by different upstream neural pathways (Fig. 1). At least two pathways have been described by Herman and colleagues (Herman et al. 1996). The limbic-insensitive pathway regulates PVN responses to "systemic or interoceptive" stressors that include immediate and threatening visceral changes such as respiratory and cardiovascular distress. These stimuli activate a direct pathway to the PVN and do not require higher-level cognitive processing associated with limbic brain regions. The limbic-sensitive pathway, by contrast, mediates PVN responses to "processive or exteroceptive" stressors and often requires not only higher-level central integration of sensory modalities but also comparisons with prior experiences to determine the salience/valence of the perceived threat. The limbic structures that project to and stimulate the PVN include the hippocampus, medial prefrontal cortex, amygdala, and BNST (Herman et al. 2005) (Fig. 2). Among these regions, the BNST has intimate and direct connections with the PVN, and the anterolateral BNST stimulates PVN and stress responding (Dunn 1987; Gray et al. 1993; Herman et al. 1994; Crane et al. 2003). Stimulation of the anterolateral BNST increases plasma corticosterone (Dunn 1987), anterior BNST lesions reduce PVN CRH levels (Herman et al. 1994), and anterolateral BNST lesions attenuate prolactin, ACTH, and corticosterone levels following a conditioned stress paradigm (Gray et al. 1993). While the BNST oval nucleus has few direct projections to the PVN (Dong et al. 2001a), this region likely increases PVN activity indirectly via projections to other BNST subregions. The posterior and medial regions of the BNST can elicit opposite effects (Dunn 1987; Herman et al. 1994), reducing PVN activity, suggesting that neuronal projections from different BNST subregions can elicit distinct stress responses. These results demonstrate the importance of the BNST in the integration and modulation of PVN activity. Perhaps more interestingly, as reviewed below, the role of the BNST in stress is even broader to encompass anxiety-like behavior to negatively valenced, diffuse, and unpredictable threatening stimuli (Fig. 1, right side) (Walker et al. 2003).
The BNST and anxiety-like behavior
In response to perceived threat, mammals display an array of defense behaviors that are adaptive for survival and the maintenance of homeostasis. The defensive responses are species- and stimulus-specific, centrally coordinated, and are often associated with changes in affect/motivation (Blanchard et al. 2003). The behavioral indices of emotion have been well studied; the defensive behaviors in rodents, such as freezing, avoidance of brightly lit areas, defensive withdrawal, and shock–probe burying, and the startle response are routinely measured and have been associated with changes in fear and anxiety-like responding (Davis 1986; Fanselow and Helmstetter 1988; Kliethermes 2005; Legradi et al. 2007). Consistent with this interpretation, experimental manipulations such as the use of m-chlorophenylpiperazine (mCPP) and benzodiazepines to increase and decrease, respectively, the experience of fear and anxiety in humans also alter the expression of these defensive behaviors in rodents. Hence, the behavioral response to homeostatic challenge likely reflects changes in emotional state, particularly in fear and anxiety. Some of the underlying neurocircuits mediating stressor-responding coincide with the neurocircuitry mediating defensive responses, and these structures (such as the BNST) appear to be critical nodes for mediating stress-induced fear- and anxiety-like behavior. Hence, chronic exposure to stressors may produce maladaptive changes within these structures, and these changes likely underlie anxiety disorders in humans.
While many CNS regions may participate in behavioral responses observed after stressor exposure, some forebrain nuclei have been argued to coordinate defensive responding in a manner similar to that described above. Of these forebrain areas, the central extended amygdala has garnered significant attention in mediating these behaviors in a variety of paradigms (Davis and Shi 1999). The central extended amygdala includes the CeA and the anatomically related BNST (Fig. 2). As noted above, the BNST has been implicated in certain fear- and anxiety-like behaviors that are not mediated by the CeA. Davis and colleagues (1997) initially found that lesions of BNST cell bodies blocked the enhanced startle responding (a behavioral measure of fear/anxiety) observed after central administration of CRH, whereas CeA lesions did not (Lee and Davis 1997). Other fear-like behaviors that have subsequently been shown to be BNST-mediated include startle responding enhanced by bright light (Walker and Davis 2002a, b), freezing behavior induced by predator odor (Fendt et al. 2003), fear responding to long-duration conditioned stimuli (Waddell et al. 2006), contextual fear conditioning (Sullivan et al. 2004), and the anxiogenic behavioral changes observed after uncontrollable stress (Hammack et al. 2004). Importantly, the BNST and CeA both receive substantial afferent information from the basolateral amygdala (BLA, Fig. 2), and both project to many of the same regions involved in mediating individual fear responses (Walker et al. 2003). Based on these data, Davis and colleagues (2003, 2009, 2010) have suggested that the BNST mediates a "slower or sluggish" tonic fear response system that mediates behavioral responding to diffuse stimuli that persists long after the stimulus has terminated. By contrast, the CeA appears to mediate a rapid phasic response system to specific threat that dissipates when the threat is removed. Davis and colleagues have likened the former to an "anxiety" response system and have suggested that the maladaptive responding of the BNST may underlie some forms of anxiety disorders in humans, including post-traumatic stress disorder (PTSD). Electrical stimulation of the anterolateral BNST region produces many of the endocrine, cardiovascular, and respiratory responses that are elicited by anxiogenic stimuli (Casada and Dafny 1991). Moreover, anxiogenic pharmacological agents, such as yohimbine and mCPP, increase BNST expression of activation markers such as c-fos (Singewald et al. 2003). The data implicating the BNST in the response to stressor exposure are not limited to rodents. Kalin et al. (2005) showed that increased BNST activity in rhesus monkeys was most positively correlated with individual differences in freezing behavior in response to eye contact with an intruder, which in this species represents a threatening stimulus (Kalin et al. 2005). The BNST has also been linked to fear behavior in humans; Straube et al. (2007) found that BNST activation was increased in spider phobic humans when they anticipated the presentation of an artificial spider (Straube et al. 2007). Notably, substantial evidence suggests that BNST activity mediates anxiety-like behavior, and altered function within the BNST likely mediates enhanced anxiety in humans. Our data suggest that chronic stress selectively increases multiple neurotrophic peptides and growth factors within the BNST, and this is consistent with previously published reports suggesting that chronic stress selectively activates the BNST (see below). Given the substantial data implicating the BNST in mediating anxiety-like behavior, we argue that the BNST is a critical site of confluence between stress responding and pathological anxiety.
Chronic stress and BNST plasticity
As noted above, stressor exposure can activate the BNST, and chronic exposure to stressors and/or pharmacological treatments (e.g., mCPP, corticosterone) have been shown to alter BNST plasticity. Several studies have found that the expression of BNST CRH was increased following prolonged social subjugation (chronic social stress), chronic "mild" stress, and chronic treatment with corticosterone (Makino et al. 1994; Watts and Sanchez-Watts 1995; Schulkin et al. 1998). In addition, these treatments have been shown to increase signs of neuroplasticity within the BNST; exposure to a chronic unpredictable stress paradigm was associated with increased BNST volume and dendritic length (Pego et al. 2008), chronic immobilization increased the number of branch points observed in the dendritic arborization of BNST neurons (Vyas et al. 2002, 2003), and a 1-week variate stress paradigm increased BNST dendritic length (May, Braas and Hammack, unpublished data). Physiological correlates to BNST neuroplasticity have also been observed, so that chronic exposure to drugs of abuse has been shown to increase excitatory postsynaptic currents in ventral–tegmental area-projecting BNST neurons (Dumont et al. 2008) as well as increase the expression of norepinephrine transporter within the BNST (Macey et al. 2003). Elevations in BNST CRH and neuroplasticity have been associated with increases in anxiety-like behavior and anhedonia (a symptom of depression, Stout et al. 2000). Hence, chronic exposure to stressors facilitates BNST function by changing neurochemistry, morphology, and physiology within this structure, and these changes are associated with increases in fear- and anxiety-like behavior. From these data, increased neuroplasticity within the BNST has been argued to mediate anxiety disorders in humans whose etiology is associated with chronic stressor exposure.
Neuropeptides and the BNST
As discussed, the anterolateral BNST and CeA have high levels of stress-related peptides, including CRH. Extrahypothalamic CRH has been heavily implicated in mediating many of the behavioral responses to stressful stimuli, including fear and anxiety (Koob and Heinrichs 1999), and CRH1 receptor knockout mice exhibit an anxiolytic behavioral profile (Timpl et al. 1998). CRH antagonists within the BNST reduce the anxiogenic response to intracerebroventricular (ICV) CRH injection (Lee and Davis 1997). Other peptides associated with anxiety and stress in the extended amygdala include CRH-related urocortin peptides, neuropeptide Y, galanin, vasopressin, and oxytocin (Walter et al. 1991; Veinante and Freund-Mercier 1997; Koob and Heinrichs 1999). As we discuss below, PACAP are well-studied pleiotropic factors and have diverse functions in development, physiology, and injury responses. From tissue distribution studies, high levels of PACAP and its cognate G-protein-coupled PAC1 receptor have been identified in the amygdala and BNST (Hashimoto et al. 1996; Hannibal 2002), particularly in CRH-rich regions. Although several studies have implicated the PACAP family of peptides in behavior and extended amygdala function, few studies have investigated their function in the BNST. Recently, our studies have shown that BNST PACAP and PAC1 receptor mRNA levels are selectively induced in the extended amygdala after chronic stress (Hammack et al. 2009). Our data demonstrating the anxiogenic properties of PACAP are consistent with behavior studies in PACAP or PAC1 receptor knockout studies (Jamen et al. 2000; Hashimoto et al. 2001; Otto et al. 2001; Colwell et al. 2004; Girard et al. 2006); further, from its trophic properties, chronic PACAP signaling may be one mechanism underlying BNST neuronal cytoarchitectural remodeling and adaptation during stress (see below).
PACAP Peptides and Receptors: A Primer
There are many excellent recent reviews on the PACAP family of related peptides (Sherwood et al. 2000; Vaudry et al. 2009) and, hence, only some of the fundamental details will be highlighted here to facilitate future discussions. PACAP, the archetypical member of vasoactive intestinal peptide (VIP)-secretin-glucagon family of bioactive peptides, was isolated from hypothalami based on its ability to stimulate anterior pituitary gland adenylyl cyclase activity (Miyata et al. 1990; Ogi et al. 1990; Arimura 1998; Vaudry et al. 2009). Two α-amidated forms of PACAP arise from alternative posttranslational processing of the precursor molecule; PACAP38 has 38 amino acid residues [pro-PACAP(131–168)] while PACAP27 corresponds to the amino terminus of PACAP38 [pro-PACAP(131–157)]. PACAP27 exhibits 68% amino acid identity with VIP (Kimura et al. 1990; Miyata et al. 1990; Ogi et al. 1990). The relative levels of the two forms of PACAP are tissue specific, although PACAP38 predominates in most tissues (Arimura et al. 1991; Arimura 1998). For example, the ratio of PACAP38 to PACAP27 can range from 500:1 in testes to 15:1 in the hypothalamus. The 28-amino acid VIP peptide is also α-amidated but, unlike PACAP, is not alternatively processed. From gene duplication, VIP and PACAP form one branch of the cladistic tree and are highly conserved among species implicating their physiological importance in evolution. For example, there is only one amino acid difference in PACAP27 between tunicates and mammals. The gene exon–intron organization, transcript untranslated regions and alternative splicing, and molecular conformation of PACAP and VIP have been reported (see Vaudry et al. 2009). Yet, despite the similarities, PACAP and VIP can be differentially expressed and regulated (Pavelock et al. 2007; Vaudry et al. 2009) and the targeted deletion of one gene does not result in compensatory expression responses by the other (Girard et al. 2006). The cloning of cDNAs encoding three distinct G-protein-coupled receptors for PACAP and VIP has provided a molecular basis for understanding the complexity of PACAP and VIP signaling (Ishihara et al. 1992; Hashimoto et al. 1993; Hosoya et al. 1993; Lutz et al. 1993; Spengler et al. 1993; Inagaki et al. 1994; Laburthe et al. 2002). Only PACAP peptides exhibit high affinity for the PAC1 receptor, whereas VIP and PACAP have similar high affinities for VPAC1 and VPAC2 receptors. While VPAC receptors appear to be coupled principally to adenylyl cyclase, PAC1 receptor isoforms display unique patterns of adenylyl cyclase and PLC activation, which differ for PACAP27 and PACAP38 (Spengler et al. 1993; Vaudry et al. 2009). Isoforms are produced by alternative splicing of the PAC1 receptor transcript regions encoding the amino-terminal extracellular domain and third cytoplasmic loop. Variants resulting from the presence or absence of a 21-residue insert into the amino-terminal extracellular domain can affect PACAP38 and PACAP27 potency (Pantaloni et al. 1996). Other variants, from the alternative splicing of two 84-bp HIP and HOP exons in the region encoding the third cytoplasmic loop, exhibit differential patterns of adenylyl cyclase and PLC activation by PACAP (Spengler et al. 1993). Stimulation of the PAC1 null receptor (neither HIP nor HOP), for example, activates adenylyl cyclase; the presence of the HIP cassette (PAC1HIP receptor) can dampen the potency and efficacy of PAC1 receptor-mediated cyclic AMP production. The PAC1HOP receptor variant can be promiscuous in Gs/Gq coupling and allow both adenylyl cyclase and phospholipase C activation for diverse downstream intracellular signaling events. These potential multifactorial PAC1 receptor signaling in adenylyl cyclase, phospholipase C, MAPK, and Akt pathways can be key in understanding neurotrophic signaling during development, plasticity, and regeneration (Barrie et al. 1997; Villalba et al. 1997; May et al. 2010). The limited number of pharmacological tools has hampered studies on the roles of the different receptor subtypes in central and peripheral tissues. While the PACAP(6–38) antagonist acts at both PAC1 and VPAC2 receptors, M65 (also called max.d.4), a 19-amino acid deletion mutant of the sand fly vasodilatory maxadilan peptide, is a potent and selective PAC1 receptor antagonist (Moro and Lerner 1997; Moro et al. 1999). Interestingly, several acyl hydrazides have now been identified as small non-peptide PAC1 receptor antagonists, but their relative selectivity at VPAC1 and VPAC2 receptors has not been described (Beebe et al. 2008). PG97-269 and PG99-465 have been developed as VPAC1 and VPAC2 receptor-selective antagonists, respectively (Vanneste et al. 2004). The chimeric, substituted peptide Lys15Arg16Leu27-VIP(1–7)/GRF(8–27) is a high-affinity VPAC1 agonist (Gourlet et al. 1997); Ro25-1553 and Hexa-VIP(1–28) are VPAC2-selective agonists (O'Donnell et al. 1994; Juarranz et al. 1999).
PACAP Peptides in Stress- and Anxiety-Related Pathways
As described previously, PACAP peptides are widely distributed in the central/peripheral nervous systems (CNS/PNS) and in peripheral organs (Vaudry et al. 2009). But among CNS structures, both PACAP and PAC1 receptor mRNA and immunoreactivity are highly expressed in limbic areas including the hypothalamus, hippocampus, olfactory nuclei, and discrete regions of the amygdala (Hashimoto et al. 1996; Jaworski and Proctor 2000; Hannibal 2002), which are well known to mediate the diverse behavioral, physiological, and endocrine responses observed following stressor exposure. Similar to CRH, some of the highest levels of PACAP mRNA expression and peptide content in the CNS are found in hypothalamic nuclei, including the PVN where PACAP can be colocalized with a subpopulation of CRH neurons (Hannibal et al. 1995). Some of the highest densities of PAC1 receptor mRNA have also been identified in the many different regions of the hypothalamus emphasizing the importance of PACAPergic systems in neuroendocrine functions and homeostasis. Interestingly, PACAP and CRH have also been identified in specific regions of the central extended amygdala, often in complementary patterns (see below), to suggest additional functional parallels. Some of the highest extrahypothalamic CRH levels have been described in the BNST and CeA (Koob and Heinrichs 1999); similarly, dense PACAP-immunoreactive fibers have been found in the dorsolateral BNST and in the capsular and central parts of the lateral CeA subdivision (Piggins et al. 1996; Hannibal 2002). In all these studies, PACAP-immunoreactive fibers and terminals are far more prevalent than PACAP-immunopositive soma suggesting that the bulk of the PACAP fibers represent extrinsic long-distance axonal projections to the CeA and BNST. The endogenous sources of the PACAP-containing axons in the PVN and BNST are still being evaluated but studies using retrograde tracers suggest that the PACAP fibers to the PVN may originate from diverse CNS regions such as local hypothalamic nuclei and more distant brainstem nuclei (Legradi et al. 1998), while those to the BNST stem significantly in part from PACAP neurons in the PVN (Kozicz et al. 1998). But in both PVN and BNST oval nucleus regions, the PACAP-immunoreactive fibers have been described to synapse on CRH neurons, implicating the two peptidergic systems in a common neural pathway neurons involved in stress responses. As specific regions of the BNST also project to the PVN, these results may also imply that the hypothalamus and BNST may have reciprocal regulatory functions. One potential caution in these observations rests in the use of colchicine in some of these studies. The microtubule polymerization inhibitor is frequently employed in many immunocytochemical peptide distribution studies to disrupt vesicle transport and secretion and enhance peptide detection in neuronal soma and fibers. As colchicine is a cellular, physiological, and behavioral stressor, and can enhance cellular mRNA and expression, its effects are clearly not solely related to vesicular transport but more complex and transcriptional. While these treatments may not necessarily distort immunocytochemical staining patterns, they may bias staining intensities from levels that are more typically observed in naive animals. Nevertheless, the sparse number of BNST PACAP-immunoreactive soma mirrors the scattering of PACAP mRNA expressing neurons in the BNST (Hannibal 2002); hence, even though the bulk of PACAP-positive fibers appear to arise from extrinsic projections, the BNST is capable of endogenous PACAP production for local and/or more long distant regulatory functions. As the cytoarchitecture of the BNST has been described to contain an inner "core" of projection neurons surrounded by an outer "shell" of interneurons (Larriva-Sahd 2006), the localization of PACAP in the BNST may have functional significance. While PACAP is more prevalent in the capsular region of the CeA, CRH-immunoreactivity patterns appear complementary and restricted to the adjacent lateral and medial CeA regions. Interestingly, even though the BLA is also a central mediator of behavioral responses, neither PACAP nor CRH fibers and soma appear prevalent in the BLA. The distribution of PACAP-immunoreactive fibers correlates well with PAC1 receptor mRNA patterns in the hypothalamus, hippocampus, and extended amygdala regions such as the BNST and CeA (Hashimoto et al. 1996). In aggregate, these results implicate PACAP signaling, via CRH-dependent and/or independent mechanisms, as one of the regulators of neuroendocrine, autonomic, and behavioral responses to stressor exposure.
PACAP Peptides in Stress-Related Behavior—Hints from Knockout Studies
Despite much evidence from neurochemical anatomy, the studies examining PACAP effects on behavior have been limited. The results from early studies evaluating the roles of PACAP in stress were modest; for example, whereas acute restraint, osmotic, and ether stress have no apparent effects, other challenges including colchicine-, interleukin-1β-, and kainic acid-induced stress can increase PACAP mRNA expression in the hypothalamus (Hannibal et al. 1995). PACAP infusions into cerebral ventricles have been shown to augment plasma corticosterone levels, stimulate c-fos and phosphorylated CREB immunoreactivity in the hypothalamus, and increase PVN CRH mRNA levels, very much similar to the physiologic responses to stress, and yet the behavioral stress responses in these animals to PACAP have only been examined with respect to grooming behavior and motor activity (Agarwal et al. 2005; Norrholm et al. 2005). Further, ICV infusion studies, while instructive, cannot typically specify the central sites of PACAP activity. Some direct nuclei microinjections/infusions have been performed; for example, PACAP infusions into the CeA result in changes in shock/probe aversion responses that are consistent with the manifestation of fear (Legradi et al. 2007).
Although these results are indicative and served as a prelude for additional studies, the ensuing behavior data from several PACAP or PAC1 receptor null mouse strains developed by several independent laboratories have also provided complementary and revealing results (Jamen et al. 2000; Hashimoto et al. 2001; Otto et al. 2001; Colwell et al. 2004; Girard et al. 2006). In general, the PAC1 and PACAP knockout animals share some defects such as hyperactive psychomotor behavior, poor fertility, circadian rhythm irregularities, and abnormalities in glucose/lipid homeostasis. Furthermore, the PACAP null mice appear to have high early postnatal mortality, which may be related to acute thermosensitivity, apnea, or other metabolic dysfunctions (Gray et al. 2001, 2002; Cummings et al. 2004a, b, 2008). Yet, despite these hurdles, some of the best evidence for PACAP/PAC1 receptor signaling in behavior has been presented in studies using these knockout animals. PAC1 receptor knockouts demonstrate abnormalities in social and sexual behavior associated with pheromone processing (Nicot et al. 2004) and appear to present deficits in contextual fear conditioning, a hippocampus-dependent associative learning paradigm (Sauvage et al. 2000; Otto et al. 2001). However, some of the most consistent and striking phenotypes in the PACAP or PAC1 receptor knockout mice are the changes in psychomotor behavior (Hashimoto et al. 2001; Otto et al. 2001; Girard et al. 2006). In open-field tests, PACAP null mice demonstrate reduced anxiety-like behavior, exaggerated jumping behavior and dramatically increased locomotor activity with little evidence for habituation to the environment. PACAP knockout animals move quicker, travel longer distances per unit time, spend less time resting, and access the center of the open field more frequently than wild-type mice, which travel preferentially along the test chamber perimeter (Hashimoto et al. 2001; Girard et al. 2006). PACAP knockouts show greater tendencies to enter and spend more time in the open arms on the elevated-plus-maze test, also consistent with a phenotype of reduced anxiety. In emergence tests, in which mice within a safe open cylinder are placed in a novel open-field environment, PACAP knockout mice demonstrate less latency emerging from the cylinder and a near 2-fold increase in exploratory times (Hashimoto et al. 2001). Other related test paradigms have also shown the peptide knockouts are less anxious and spent more time exploring novel objects. The same psychomotor behaviors have been observed in PAC1 receptor knockout mice. Interestingly, unlike mice with a global PAC1 receptor deficiency, the PAC1CaMCRE2 mice with targeted disruption of cortical and hippocampal PAC1 receptors did not present psychomotor behavioral defects (Otto et al. 2001), suggesting that PACAP signaling outside of these areas, such as the extended amygdala, may control the anxiety responses. The hyperactive behavior the PACAP null animals can be ameliorated with the dopamine antagonist haloperidol and the explosive jumping behavior can be attenuated with serotonin reuptake inhibitors. While the monoaminergic system does not appear to be perturbed in embryonic knockout brains, cortical and striatal 5-HIAA (a serotonin metabolite) may be diminished slightly in adult PACAP-deficient animals, which implicates a late developmental role for PACAP in serotoninergic system function. Other stress-related responses are also attenuated in PACAP knockout animals. Intraperitoneal injections with trimethyltin to instill neuronal damage and systemic stress failed to induce corticosterone levels in knockout animals compared to wild-type (Morita et al. 2006). More recently, the increase in hypothalamic CRH mRNA and serum corticosterone observed in wild-type mice following prolonged restraint stress has been shown to be blunted in PACAP-deficient mice (Stroth and Eiden 2009). As a caution, analogous behavioral studies have not been performed using conditional knockout animals. Clearly, maternal gestational influences and even postnatal handling can impact development, and these issues should be considered as additional animal resources become available. But, despite the many related observations suggesting that PACAP modulates anxiety-like behavior and stress responding, the neuroanatomical substrates, characteristics, and mechanisms of PACAP action have not been identified. Our recent studies suggest that one primary locus for PACAP signaling in anxiety-like behavioral responding to stressor exposure resides in the BNST and that the ensuing long-term changes in PACAP expression may underlie the long-lasting neurological and physiological defects that may have permanence in allosteric load.
Chronic Variate Stress Increases PACAP, PAC1 Receptor, and Neurotrophin-Related Transcripts Expression in the BNST
Chronic stress elicits diverse neurotransmitter and hormonal responses through activation of multiple signaling pathways, including SAPK/JNK (Shen et al. 2004), one critical regulator of neuronal PACAP expression following metabolic stress. To evaluate whether chronic stress regulates PACAP expression in brain regions associated with stress-responding and/or anxiety-like behavior, Sprague–Dawley rats were exposed to a chronic variate stress paradigm in which rats received a different stressor in each of 7 days to reduce habituation of the stress response (Hammack et al. 2009). Twenty-four hours after the last stressor, several different brain regions associated with stress and fear behavior were microdissected and frozen on dry ice before RNA processing for quantitative RT–PCR measurement. As reported in Hammack et al. 2009, among the 12 neural regions examined, chronic variate stress selectively increases PACAP transcript levels more than 10-fold only in the dorsolateral BNST (dorsal aspect of anterolateral BNST); a smaller but significant 2-fold increase in PACAP mRNA is also apparent in the hypothalamic PVN. PACAP levels in the remaining brain regions, including the central and basolateral amygdala, and ventral aspect of the BNST, are not different from non-stressed control animal tissues. The stress-induced increase in dorsolateral BNST PACAP expression is associated with a 2-fold increase in PAC1 receptor mRNA expression; like all CNS tissues examined to date, the PAC1null receptor isoform predominates in the BNST. The increase in dorsolateral BNST PACAP and PAC1 receptor appears unique as VIP, VPAC1, and VPAC2 receptor transcript levels in the same samples are not changed (Hammack et al. 2009).
Within the same tissue sets, the chronic variate stress paradigm also augmented other stress-related transcripts in the PVN and amygdala, some of which may have been consequences of PACAP signaling. For example, chronic variate stress also increased brain-derived neurotrophic factor (BDNF) and TrkB mRNA levels nearly 3-fold and 2-fold, respectively, in the dorsolateral BNST when compared with non-stress control tissues. PACAP can stimulate neuronal BDNF and/or TrkB expression and function in a variety of paradigms (Yaka et al. 2003; Braas et al. 2007) and CNS BDNF expression appears diminished in PAC1 receptor knockout animals (Zink et al. 2004). Since chronic stress results in long-term changes in dorsolateral BNST cellular plasticity, and BDNF function has been associated with anxiety and behavior disorder, PACAP-stimulated BDNF expression may be one mechanism underlying that plasticity. To that effect, PACAP treatment of dorsolateral BNST explants in serum-free cultures can increase BDNF transcript expression (unpublished observations). BDNF transcripts in a few select CNS regions are also increased following chronic variate stress, including the PVN (approximately 1.4-fold) and dorsal raphe nucleus (3-fold). As these CNS areas are targets of BNST projections, the observed changes in BDNF and TrkB transcript expression in these regions may also reflect stress-mediated PACAP production and signaling from the BNST. Importantly, these data suggest that the dorsolateral BNST is a critical CNS target of stress-induced plasticity, and such plasticity within the BNST may represent a likely mechanism underlying anxiety disorders in humans. It is notable that neither PACAP nor BDNF was increased in the BLA, which like the BNST can exhibit enhanced neuroplasticity after some chronic stress paradigms (Vyas et al. 2002). These data might suggest that BLA enhancements in neuroplasticity are not PACAP dependent; however, it is currently unclear whether the chronic variate stress paradigm enhances BLA neuroplasticity, as Vyas and colleagues (2002) only found enhanced neuroplasticity in the BLA following chronic immobilization stress and not after a chronic unpredictable stress paradigm.
As in other stress paradigms, the same chronic variate stress treatment also increases CRH transcripts in the PVN. Though BNST CRH transcript level appears unchanged in this paradigm, expression of the different BNST CRH receptor subtypes is enhanced following chronic stress. Interestingly, the greatest increase in CRH mRNA is noted in the lateral and medial CeA which may be related to fear-like responses. Again, as PACAP-immunoreactive fibers can impinge and regulate CRH neurons, and as stress-induced expression of hypothalamic CRH is diminished in PACAP knockout animals, these results further implicate an integration of PACAP and CRH pathways.
Chronic Variate Stress Increases PACAP Immunoreactivity and Transcript Levels in the Oval Nucleus of the BNST
Acute PACAP Injection into the BNST Induces Stress-Related Behavioral Consequences
The ability of chronic variate stress to selectively increase BNST PACAP and PAC1 receptors transcripts has suggested that this system plays an important role in chronic stress-mediated anxiety-like behavior. These observations, coupled with other PACAP-related stress studies and the anxiolytic behavioral changes observed in the PACAP and PAC1 receptor knockout mice, in aggregate implicate BNST PACAP signaling as a potential mechanism for anxiogenic responses and the long-term neuroplasticity changes that accompany anxiety-like behavior. To evaluate that possibility, adult male rats were implanted bilaterally with cannula aimed at the anterior BNST and subsequently infused with one of several PACAP38 doses (0.1–1 μg) or vehicle at a flow rate of 0.25 μl/min. Consistent with hypotheses, PACAP38 was anxiogenic in a concentration-dependent manner as measured by increased baseline startle behavior (Hammack et al. 2009). Perhaps more interestingly, BNST-treated rats continue to exhibit an elevation in baseline startle amplitude even 1 week after the single PACAP38 injection. As PACAP can elicit sustained neurotrophic effects, these results suggest that PACAP-induced BNST neuroplasticity may be one mechanism underlying the long-term elevation in anxiety-like behavior.
Although BNST PACAP signaling may be anxiogenic, whether chronic stress-induced anxiety is mediated by central PACAP functioning is currently under study. In preliminary work, the rats were infused continuously into the lateral ventricles with vehicle or the PAC1/VPAC2 antagonist PACAP(6–38) via osmotic minipumps (1 μl/h, 12 μg/day) during the 7-day chronic stress paradigm, and 24 h after the last stressor, rats were tested for anxiety-like behavior on an elevated plus maze. While the antagonist-treated animals appeared to venture into the open arms more frequently in these preliminary studies, the results on anxiety-like behavior were equivocal from variability within the small animal groups. However, in the same study, chronic variate stress, previously shown to produce anorexia in rodents, dramatically reduced weight gain more than 70%. Interestingly, chronic central PACAP(6–38) antagonist infusion dramatically reversed the stress-induced weight change such that the body weights of stressed/PACAP(6–38) treated animals were comparable to those of non-stressed controls. These antagonist responses were so dramatic that additional studies were performed to identify the sites and roles of PACAP in weight change. Recently, in assessing the role of the BNST in stress-mediated weight change, excitotoxic N-methyl-d-aspartate BNST lesions were performed prior to chronic stress treatments. In parallel with the PACAP antagonist infusion studies, chronic stress-induced weight loss was reduced in the BNST-lesioned animals compared to sham or non-stress control animals, demonstrating that the BNST is an important site for stress-induced anorexia. To determine whether BNST PACAP alone was sufficient to produce anorexia in the absence of stress, PACAP38 (0.1–1 μg) was injected directly into the BNST, and within 24-h post-infusion, PACAP dose-dependently produced a dramatic reduction in weight and food/water intake. Hence, in addition to anxiety-like behavior, these results suggest that intra-BNST PACAP expression and signaling represent an important locus for weight/feeding regulation and the anorexic effects of stress.
Summary and Overview
The many separate lines of work are beginning to coalesce and implicate PACAP expression and signaling in stress-related behaviors. To encapsulate our recent observations, our work suggests that PACAP/PAC1 receptor signaling has acute and sustained stress-associated behavioral effects when injected into the BNST. PACAP and PAC1 receptor expression is augmented selectively in the BNST after chronic stress, particularly in BNST subregions that express stress-related CRH. BNST CRH activation has been shown to be necessary and sufficient for the expression of anxiety-like behavior, and the distribution and functional similarities between the two peptidergic systems suggest that the PACAP and CRH pathways may be integrated to increase BNST activity and coordinate these behavioral changes. As noted above, the increase in BNST neuroplasticity has been argued to represent a key underlying mechanism to sustain behavioral changes, such as anxiety after chronic stress. In addition to its transmitter activities, PACAP has well-established neurotrophic functions through G-protein-coupled PAC1 receptor function or downstream induction of neurotrophins, especially BDNF. As chronic stress and PACAP can upregulate BDNF and TrkB expression, PACAP may be an important mediator of stress-induced increases in BNST neuroplasticity. Hence, the effects of PACAP may be multidimensional with other transmitters, peptides, and growth factor systems to enhance not only acute but also long-term stress-induced behavioral changes. These studies have the potential of defining specific mechanisms for the etiology of anxiety disorders with important implications for clinical therapeutic adaptations. PACAP systems have also been implicated in depression and schizophrenia-like disorders (Hashimoto et al. 2008, 2009a, b). Although not directly associated, depression and anxiety are two of the most comorbid disorders known (Simon 2009); the presence of anxiety in schizophrenia-like disorders is also highly prevalent (Achim et al. 2009). Future PACAP studies may identify other clinical correlations with chronic debilitating anxiety, PTSD, anorexia-like behavior, and related feeding-related disorders.
This work was supported by grants HD27468 and NS37179 (VM and KMB), and MH072088 (SEH) from the National Institutes of Health. Portions of the work were also supported by the National Alliance for Research on Schizophrenia and Depression (NARSAD). The use of the Molecular Biology Core Facility at the University of Vermont College of Medicine supported by National Institute of Health NCRR P20RR16435 is also gratefully acknowledged.

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Don't miss
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Smasne Cellars 2010 Konner Ray Red, Columbia Valley, $50
By Great Northwest Wine on January 3, 2014
Last year's Washington Winery of the Year for Wine Press Northwest magazine continues to impress with this special blend named for his young son. The blend of Bordeaux varieties from Verhey, Phinny Hill and Upland vineyards leads with Malbec (51%) and followed by substantial support from Cabernet Sauvignon (42%), Petit Verdot (4%) and Carmenere. Aromas offer up hints of cranberry, raspberry and dried herbs, along with vanilla, rosehip, ginger and vanilla. Gobs of ripe red fruit flavors are met with a bold tannin structure, while racy acidity and notes of juniper berry and cardamom extend the finish.
Rating: Outstanding!
Production: 70 cases
Alcohol: 13.9%


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REVISED: Youth Alter Servers Schedule thru October: Schedule
Current Events and Calendar
Monthly Calendar: August Parish Calendar September Parish Calendar Current Events: Parish Picnic: Save the date! Sunday, Sept. 18th, 12:00 – 4:00 P.M. St. Joseph Parish Social Hall and outdoor grounds. If you are interested in helping, but did not sign up for the ministry, we would love to have you join us too. We …View full post
Women's Renewal
"Come to the Water" Ladies, please join us for a Women's Renewal, at St. Joseph Parish in Amherst On October 22 & 23, 2016 Open to the Women of St. Joseph, Nativity BVM, Sacred Heart (Oberlin) & St. Patrick Check-in begins Sat., Oct. 22 at 7 am. Renewal begins at 8 am We will conclude …View full post
P.S.R. Program
PARISH SCHOOL OF RELIGION (P.S.R.) Registration for the 2016-2017 PSR year is NOW open! Registration forms can be found below or are available in parish office during regular business hours beginning June 1, 2016. PLEASE pay attention to the registration deadline, the deadline to register for the 2016-2017 PSR year is September 1! …View full post
2016 Benefit Raffle
Dear Parishioners and Friends of St. Joseph's, Yes, the raffle tickets for the 2016 annual raffle are now available. As of today, over $422,200.00, has been won by you and those who have bought tickets from you. The cost is $25.00, a ticket. You have 120 chances to win in 2016! You must be 18 …View full post
Stewardship Council
Mission: To develop a parish Stewardship plan that will allow each St. Joseph parishioner to be challenged to reflect on God's blessings and then prayerfully consider how God wants their talents to be used for service through and in the best interest of St. Joseph Parish. Talents Needed: Planning, implementation, creativity, telephone skills, as well …View full post
Electronic Offertory Now Available!
St. Joseph Church has teamed up with myEoffering to enable parishioners to give your weekly offering electronically from your bank account or credit / debit card in place of using a paper envelope. You can opt to make a one-time gift, if you are out of town or ill on a particular weekend …View full post
Fr. O'Connor's Homily: August 28th, 2016
Twenty-second Sunday in Ordinary Time-C
Sirach3: 17-18, 20, 28-29
Hebrews 12: 18-19, 22-24a
Luke 14:1, 7-14
Aesop tells a fable about a frog that wanted to fly. One day a stork landed in the cove and the frog had an idea. The stork was looking for minnows, but the frog's noisy voice had driven them all away. So the frog offered the stork a deal: "If you help me fly, I will show you where the minnows' secret hiding place is."
The deal was made. The frog betrayed his minnow neighbors and the stork had a feast. Then the stork asked the frog, "Now, how am I going to help you fly?"
The frog said, "I'll just take hold of one of your legs with my mouth and then as you fly, I can go with you." And it worked out perfectly.
People on the ground looked up and saw the stork flying with the frog on his leg and they were marveling. One of them said, "I wonder which one of those animals came up with that brilliant idea?"
The frog opened his mouth to say, "It was entirely my idea." And the consequence of his pride caused the frog to plummet to the earth.
And Aesop gives us this moral to the story: "Pride precedes the fall."
We know that to be true, for pride precedes our falls as well. Pride attacks us when we are successful and we begin congratulating ourselves. Pride accepts no criticism. Pride sees everyone else as a subordinate. Pride expects to be on a par with God – or even above Him!
In the early days, the Fathers of the Church put pride at the top of the list of the seven deadly sins: pride, covetousness, lust, anger, gluttony, envy and sloth.
The Scriptures today speak about humility. The first reading from the Old Testament, the Book of Sirach, has this line: "Children, conduct your affairs with humility, and you will be loved more than a giver of gifts." And isn't that true? Humble people are wonderful people to be around.
In the Gospel Jesus teaches us about humility. He talks about a wedding banquet: those who would seek the place of honor at the table and then are moved to a lower place, and those who would seek the lowest place and be invited to come higher. Jesus says to us, "Those who exalt themselves will be humbled, but those who humble themselves will be exalted."
Imagine how refreshing your work place or school or social circle would be if there were no more games of one-upsmanship, or posturing to be noticed, or worrying about networking with the powerful and popular for personal advantage.
Jesus is teaching us a new way of life where we are not competitors but companions on the journey, where life is not a castle to be conquered but a banquet to be shared, where we do not need to struggle and grab for power because power is only to be used to serve other people. And Jesus mentions some of them in today's Gospel: "the poor, the crippled, the lame and the blind."
Now you may think that we are making a little too much of first-century table etiquette. But may I remind you that character is formed and character is revealed in the little things.
In many job interviews there is a golf game or a meal out. Why? Because our character comes through especially at moments when we think that nobody is watching. The ways that we treat the most invisible people in society reveal what we think of human society.
The little things are important. And a table is a good place to start, and that is where Jesus teaches us in today's Gospel.
In the legend of King Arthur and the Knights of the Round Table, there is a powerful lesson in the shape of that table. There was no head or foot. Rather, it was round. Every knight mattered and could have a place at that table.
In His humility, Jesus chose to be with us at His table, at this altar. Here we are nourished with His Word in the Scriptures and with His Body and Blood in the Eucharist. Here everyone matters and everyone can have a place.
It is here that we grow together as one family in Christ. For we all need His grace, His mercy and His providential care.
"Those who exalt themselves will be humbled, but those who humble themselves will be exalted."
"Children, conduct your affairs with humility, and you will be loved more than a giver of gifts."
Fr. O'Connor's Homily: August 21st, 2016
Twenty-first Sunday in Ordinary Time-C
Isaiah: 66: 18-21
Hebrews 12: 5-7, 11-13
Luke 13: 22-30
Someone asked Jesus in today's Gospel, "Lord, will only a few people be saved?" And He answered, "Strive to enter through the narrow gate, for many, I tell you, will attempt to enter but will not be strong enough."
A writer diagrammed Jesus' response this way. Think about a triangle without a base – like a teepee – and that open space at the bottom is a door that is very wide. You can enter quite easily, but the further you get in, the more confined and compressed you are. It looks like it offers absolute freedom, but once inside your freedom is seriously limited.
That same writer then said that if we think about what Jesus is teaching us in today's Gospel, the diagram would look like a "V" with a very narrow entrance at its base. It is difficult to get in, but possible. And once you get in, the promises and possibilities are immensely widened.
The door to eternal life is a narrow door. "Strive to enter through the narrow gate," Jesus teaches us.
Many of you are going back to school this week. Education is a narrow gate. If you had a wonderful summer, the temptation is to not go back to school and to prolong the leisure. But where would that lead you in the long run?
"Enter through the narrow gate." Go to school and work hard. Seize the opportunities that come your way. Don't just get by. Strive to excel, using all of your abilities. It will pay off by opening wide possibilities for your future.
Now, when you have finished school, having gone through the narrow gate, and if you still want to work for a minimum wage, you can! But there are lots of better choices that you will be able to make. Education is a narrow gate, and it pays off.
Physical fitness is a narrow gate. That may be an unexpected topic to bring up in church. But God made our bodies as well as our souls. And one day these bodies of ours that will die are going to be re-united with our souls as they are raised up in glory to everlasting life, as we profess in the Creed each Sunday. The Lord expects us to take proper care of our bodies – not over-indulging them, not neglecting them, and always respecting them.
Someone said that his original goal in life was to have a body that looked like a Greek god. But later on in life he actually looked more like a Greek restaurant! Yes, neglect takes its toll.
Marriage is a narrow gate. Those of you who are married probably had several possibilities for a spouse, but you chose the one that you married. Eliminating all of the others for the one person that you are with can sound so limiting. Yet in a graced, faithful marriage look at all of the abundant blessings that come to be.
A little girl had a doll collection. She was asked which one was her favorite. She went to her room and came out with a doll that even Goodwill would have rejected. Most of the hair had come off, one eye was missing and the dress was tattered.
When she was asked why this one was her favorite, she answered: "Because if I don't love this dolly, nobody will."
Well, there is not a single one of us that is outside of God's circle of mercy and love. "God loves each one of us as if there were only one of us to love," as Saint Augustine wrote.
The narrow gate leads to abundant life whether we are talking about education or physical fitness or marriage or anything else. And the most important of these narrow gates is the one that leads to heaven.
There is room for each one of us at the narrow gate that leads to eternal life. But we must make the choice to enter it.
"Strive to enter through the narrow gate," Jesus teaches us. And be blessed with abundant life here and herafter.


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Native Plants
Q. Who is Mr. Smarty Plants?
A: There are those who suspect Wildflower Center volunteers are the culpable and capable culprits. Yet, others think staff members play some, albeit small, role. You can torture us with your plant questions, but we will never reveal the Green Guru's secret identity.
Did you know you can access the Native Plant Information Network with your web-enabled smartphone?
Ask Mr. Smarty Plants is a free service provided by the staff and volunteers at the Lady Bird Johnson Wildflower Center.
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Thursday - February 07, 2013
From: Spicewood, TX
Region: Southwest
Topic: Grasses or Grass-like
Title: Unrecognized grass in Habiturf from Spicewood TX
Answered by: Barbara Medford
QUESTION:I purchased 2 bags of Habiturf from the Wildflower Center and planted it in late September. Now, early February, the predominant grass is not any of the 3 supposed components of the Habiturf, but looks more like perennial rye. Is it possible that the Habiturf had that seed in it? It is perhaps 80% of the lawn..now with flowering seed heads all over.
Actually, the Habiturf mix has four native grasses in the mixture: Bouteloua dactyloides (Buffalograss), Bouteloua gracilis (Blue grama), Bouteloua hirsuta (Hairy grama) and Hilaria belangeri (Curly mesquite grass). Below are three pictures of each grass, in some cases dried specimens from herbariums, so you can see all the details of the seeds and stalks. You can click on any picture and it will take you to an enlarged view of that picture in our Image Gallery. Also, you can click on any of the 4 plant links above to our Native Plant Database webpage on that plant, and get the details of height, planting and maturation times.
Next, if we may ask - did you read the articles and see the videos we have on installation of Habiturf, including preparation of the site in advance and practices in sowing the seeds? Please read these articles and check the instructions and seasons to see if you were in sync:
Habiturf - The Ecological Lawn
As we re-read those articles, it appears to us that in the first place, the recommended planting time in Central Texas is Spring, not September. Going along with that, rye grass is frequently planted as a cover grass. If the ground has not been sufficiently prepared with tilling and application of compost as the articles suggested, the rye may have come back and taken over in the Summer before your grass seeds were planted in the Fall. Be sure to watch the video on installing Habiturf.
Hopefully, if it is properly cared for and mowed, the Habiturf will be able to overtake the rye grass (if that is what it is) and out-compete with it.
From the Image Gallery
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The annual Shelbyville Horse Show Jubilee Breakfast went off without a hitch Thursday morning in spite of a rainy start to the day.
The rain did not dampen the spirits of the crowd of more than 200 people as they filed into the huge barn at Undulata Farm for the breakfast at 7:30 a.m., while host Edward "Hoppy" Bennett stood by watching and sipping coffee.
"This rain had me worried, but everything is turning out okay," he said.
A candidate's forum Tuesday night sponsored by Shelby County Farm Bureau gave both candidates for state representative the chance to air their views and expound on their platforms.
The event, held at the Stratton Center, drew a crowd of about 60 people, said Kentucky Farm Bureau Agency Manager Pat Hargadon.
"We were quite pleased with the turnout," he said, adding that both Rob Rothenburger and Cyndi Powell-Skellie were in attendance.
Although attended by only two residents, members of the fairness group Shelby County Kentuckians for the Commonwealth say they are pleased with a forum held Wednesday night to address the issue of raising the minimum wage.
The event, held at the Stratton Center, featured speaker Dustin Pugle from the Kentucky Center for Economic Policy.
Five years ago, the Shelby County Fiscal Court opted to close the Bailey bridge, but one resident hopes to see traffic return to the bridge once again –foot traffic, at least.
Walter Laughlin said the thought of such a historic bridge falling further into disrepair was disheartening. Laughlin saw the bridge as a tourism promotion opportunity.
"It's a natural tourist attraction," he said, noting that until the early 1900s, the bridge was a covered walking bridge and he wants to see it returned to its former state.
Final preparations are underway for The Shelbyville Horse Show, which kicks off Wednesday night and runs through Saturday.
Organizers say the 27th annual horse show will draw thousands each night for both the show and the fun, fellowship and food on the sidelines.
"We expect as good or a better show than ever," said R.H. Bennett, the Shelbyville Horse Show manager.
Gates open at 6 p.m. each day, with the show starting at 7 p.m. More than 300 horses are expected to compete in nearly 60 classes over the 4-day period.
Tammy Redmon lives a quiet life; she has never been nationally recognized or cited for any daring act of heroism.
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Still, she preseveres with the help of a specially equipped van with which she can travel to necessary errands, such as doctor's appointments.
This year's Shelbyville Horse Show Jubilee promises to be a great event with something for everyone, organizers say.
Eilene Collins, executive director of Shelby Main Street, said Jubilee festivities kick off Thursday with the annual breakfast at Undulata Farm Thursday morning at 7:30 a.m.
Collins said more than 200 tickets for the event have been sold.
This year's speaker for the breakfast is noted local horse trainer Lionel Ferreira, trainer of 5-gaited world's grand champion horses.
On Saturday, Aug. 13, concerned residents and churches of Shelby County will host a March to Recovery to bring awareness to drug addiction and drug-related deaths in Shelby and surrounding counties. The March to Recovery is a kick-off to a large-scale assault on addictions of all kinds in the region.
The March will begin at 10 a.m.
On Thursday the Shelby County Board of Education will hear an update from Clear Creek Principal Kim Willhoite on Innovation at Clear Creek – The Summit. District Public Relations Coordinator Ryan Allan said The Summit is Clear Creek's 3PT (Pace, Place, Path and Time) program.
"It's a personalized learning concept we're seeing across the county," Allan said, explaining that Clear Creek is one school in the district that will be piloting a 3PT program in the district.
The Summit will involve personalized, self-paced learning.
In a brief meeting Thursday, the Shelbyvill City Council covered a light agenda, which included the annexation of property into the city limits. The board voted unanimously, with board members Mike Zoeller and Shane Suttor absent, to annex into Shelbyville a .975-acre tract of property on the south side of U.S. 60, west of Shelbyville city limits, where the existing Zaxby's restaurant is located.
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The Sentinel-News is your source for local news, sports, events and information in Shelby County and Shelbyville, KY, and the surrounding area.


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Motorists in Marlborough forked out nearly $1.2 million on parking last year, a new report shows.
In full flight, virtually
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Immigration Minister says employment breaches could result in sanctions against overseas recruitment.
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Candidates have their say
In the lead-up to the local body elections we asked council candidate Cynthia Brooks to talk about her vision for Marlborough
We're a happy bunch
1:19 PM But some residents feel the council does too much behind closed doors.
Love in a bleak place
Michael Fassbender wanted no part of filming on an isolated NZ coast, but then he felt the light of love.
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Daily Archives: June 6, 2011
AW June Blog Chain: Set a Scene!
Self-explanatory, and an excerpt from Book 2 is behind the cut. :) Notabene: would make a lot of sense if you've been to NYC's Penn Station.
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