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Final

NEUR 3304 Study Guide - Final Guide: Cortisol, Wild Type, TryptophanPremium

10 pages167 viewsFall 2016

Department
Neuroscience
Course Code
NEUR 3304
Professor
Elizabeth Nisbet
Study Guide
Final

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NEUR 3304 Final Study Notes
Molecules
POMC: pro-opiomelanocortin
oPrecursor peptide synthesized in the pituitary gland and arcuate
nucleus of hypothalamus
oCleaved into multiple hormones including: a-MSH in the arcuate
nucleus, ACTH in the adrenal cortex and B-endorphin throughout the
brain
oAxons of ghrelin cells project to POMC circuits
oOne of two main feeding inhibitory signalling molecules
oExtremely elevated levels of leptin cause release into PVN and LHA as
a-MSH, which then acts on MC3/4 receptors to decrease food intake
oPOMC ARC neurons have leptin receptors
oNucleus of the solitary tract also has POMC receptors
oIncreased expression in response to PYY
NPY: Neuropeptide Y
oOne of two orexigenic anabolic peptides, therefore involved in feeding
stimulatory circuit
oAxons of ghrelin cells project to NPY producing circuits
oDirectly signals the PVN to promote feeding
oLow levels of leptin result in increased release into the PVN via
stimulation of NPY producing neurons in the ARC
oReciprocal interaction with CRH in the hypothalamus, thus stress can
cause dysregulation and can lead to overeating and obesity
oNucleus of the solitary tract also has NPY receptors
oPYY inhibits NPY release in hypothalamus which leads to decreased
food consumption and increased expression of POMC
oIncreased long term within the ARC by stress
AgRP: Agouti-Related Protein
oOne of two orexigenic anabolic peptides, therefore involved in feeding
stimulatory circuit
oAxons of ghrelin cells project to AgRP producing circuits
oAgRP indirectly promotes feeding by blocking MC4 receptors in the PVN
oLow levels of leptin result in increased release of AgRP in the PVN to
increase feeding
oNucleus of the solitary tract also has AgRP receptors
oPYY inhibits AgRP release in hypothalamus which leads to decreased
food consumption and increased expression of POMC
oIncreased long term within the ARC by stress
a-MSH: alpha-melanocyte stimulating hormone
othe main anorectic and catabolic neuromodulator produced through
the cleavage of POMC in the ARC, thus is a main part of the inhibitory
feeding signals
oacts primarily via MC4 and some MC3 in the PVN to inhibit feeding
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CART: cocaine and amphetamine related transcript
oOne of the two main signalling molecules in the inhibitory feeding
circuit
oSecreted from the same ARC neurons that secrete POMC/a-MSH to the
PVN and LHA of the hypothalamus
oCART neurons have leptin receptors and thus high levels of leptin
induce greater CART gene expression
oNeurons also have axons to brain and spinal cord regions involved with
autonomic nervous system regulation
oIncreases metabolic rate (catabolic)
MCH: melanin-concentrating hormone
oNeurons located in the LHA and are critical to body mass regulation
oRelease is stimulated via NPY tracts from the ARC
oMCH receptor deletion in knockout mice have increased food intake as
well as increased energy expenditure (which re7ects altered
metabolism and hyperactivity)
PP: pancreatic polypeptide
oOne of two satiety signals that increase in response to food intake
oMay regulate time between meals independent of ghrelin and leptin
oModulates secretion of glucagon and insulin, and secreted from islets
of langerhans
PYY: peptide YY/peptide tyrosine tyrosine
oOne of two satiety signals that increases in response to food intake
odecreases food intake by inhibiting hypothalamic NPY- and AgRP
expressing neurons which releases their inhibition of neighbouring
POMC-expressing neurons
oreleased by distal sections of the digestive tract
osecreted in proportion to caloric intake, and e8ects are longer lasting
than CCK
Orexin
oAnabolic molecule released in the LHA
oComes in two forms, A and B
oA form increases food intake possibly by inhibiting sleep
2DG: 2-deoxyglucose
oGlucose metabolism inhibitor
oNeurons in the caudal brain stem (especially the area postrema and
the NST) show an increase in activity when rats are treated with 2DG
leading to hyperphagia
Ghrelin
oHunger inducing hormone produced within GI tract after prolonged
absence of food and/or in anticipation of meals
oAxons of ghrelin cells project to NPY, CART, POMC and AgRP circuits in
ARC
oWorks in opposition to leptin; concentrations are inversely correlated
and tightly associated with regulation of energy balance, food intake,
and body mass
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oPlasma levels increased by stress
Leptin
opredominantly produce from white adipose cells
oencoded for by ob gene
oARC has highest concentration of leptin receptors
oElevated leptin levels signal the hypothalamus that fat stores are
increasing which inhibits eating and signals the reproduction system
that it is good to go, stimulating POMC/CART circuits
oincreases at the end of meals and act as satiety signals that reduce
food intake
ocentral injection increases energy expenditure
oPlasma leptin expression is positively correlated with body fat mass
oLeptin can increase free fatty acid oxidation and prevent storage of fat
fuels in the form of triglycerides
oExogenous leptin seems to a8ect reproduction via indirect e8ects on
fuel oxidation
ADH: antidiuretic hormone
oEquivalent to vasopressin
oreleased from posterior pituitary controls water uptake from collecting
duct of kidney nephrons, thus has role in osmoregulation
oreleased in response to hypovolemic thirst detected by baroreceptors
in blood vessels
GOAT: ghrelin O-acyltransferase
oEnzyme that activates the precursor molecule of ghrelin, allowing for
ghrelin to have e8ect
oNovel target for modulation as potential treatment of obesity, as
reduction in GOAT e8ect reduces ghrelin and in turn reduces eating
levels
MTII
oMC3/4 agonist
oWhen given to subjects, results in reduced consumption of food, as
replaces the e8ect of a-MSH
Aldosterone
osecreted by adrenal gland
ocontrols uptake of sodium by stimulating sodium pumps in ascending
limb of loop of Henle on kidney nephrons, thus has role in
osmoregulation
oalso acts at mineralocorticoid receptors in the brain to stimulate salt
appetite
Renin
oEnzyme released by the kidney in response to low blood pressure
oCauses the conversion of angiotensinogen to vasconstricting
angiotensins
Angiotensin I, II, III
oVasoconstrictor molecules converted from angiotensinogen by renin in
response to low blood pressure detected by the kidney
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