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Final

NEUR 3304 Final: Final Notes
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10 Pages
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Fall 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
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
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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Description
NEUR 3304 Final Study Notes Molecules  POMC: pro-opiomelanocortin o Precursor peptide synthesized in the pituitary gland and arcuate nucleus of hypothalamus o Cleaved into multiple hormones including: a-MSH in the arcuate nucleus, ACTH in the adrenal cortex and B-endorphin throughout the brain o Axons of ghrelin cells project to POMC circuits o One of two main feeding inhibitory signalling molecules o Extremely elevated levels of leptin cause release into PVN and LHA as a-MSH, which then acts on MC3/4 receptors to decrease food intake o POMC ARC neurons have leptin receptors o Nucleus of the solitary tract also has POMC receptors o Increased expression in response to PYY  NPY: Neuropeptide Y o One of two orexigenic anabolic peptides, therefore involved in feeding stimulatory circuit o Axons of ghrelin cells project to NPY producing circuits o Directly signals the PVN to promote feeding o Low levels of leptin result in increased release into the PVN via stimulation of NPY producing neurons in the ARC o Reciprocal interaction with CRH in the hypothalamus, thus stress can cause dysregulation and can lead to overeating and obesity o Nucleus of the solitary tract also has NPY receptors o PYY inhibits NPY release in hypothalamus which leads to decreased food consumption and increased expression of POMC o Increased long term within the ARC by stress  AgRP: Agouti-Related Protein o One of two orexigenic anabolic peptides, therefore involved in feeding stimulatory circuit o Axons of ghrelin cells project to AgRP producing circuits o AgRP indirectly promotes feeding by blocking MC4 receptors in the PVN o Low levels of leptin result in increased release of AgRP in the PVN to increase feeding o Nucleus of the solitary tract also has AgRP receptors o PYY inhibits AgRP release in hypothalamus which leads to decreased food consumption and increased expression of POMC o Increased long term within the ARC by stress  a-MSH: alpha-melanocyte stimulating hormone o the main anorectic and catabolic neuromodulator produced through the cleavage of POMC in the ARC, thus is a main part of the inhibitory feeding signals o acts primarily via MC4 and some MC3 in the PVN to inhibit feeding CART: cocaine and amphetamine related transcript o One of the two main signalling molecules in the inhibitory feeding circuit o Secreted from the same ARC neurons that secrete POMC/a-MSH to the PVN and LHA of the hypothalamus o CART neurons have leptin receptors and thus high levels of leptin induce greater CART gene expression o Neurons also have axons to brain and spinal cord regions involved with autonomic nervous system regulation o Increases metabolic rate (catabolic)  MCH: melanin-concentrating hormone o Neurons located in the LHA and are critical to body mass regulation o Release is stimulated via NPY tracts from the ARC o MCH receptor deletion in knockout mice have increased food intake as well as increased energy expenditure (which reflects altered metabolism and hyperactivity)  PP: pancreatic polypeptide o One of two satiety signals that increase in response to food intake o May regulate time between meals independent of ghrelin and leptin o Modulates secretion of glucagon and insulin, and secreted from islets of langerhans  PYY: peptide YY/peptide tyrosine tyrosine o One of two satiety signals that increases in response to food intake o decreases food intake by inhibiting hypothalamic NPY- and AgRP expressing neurons which releases their inhibition of neighbouring POMC-expressing neurons o released by distal sections of the digestive tract o secreted in proportion to caloric intake, and effects are longer lasting than CCK  Orexin o Anabolic molecule released in the LHA o Comes in two forms, A and B o A form increases food intake possibly by inhibiting sleep  2DG: 2-deoxyglucose o Glucose metabolism inhibitor o Neurons 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 o Hunger inducing hormone produced within GI tract after prolonged absence of food and/or in anticipation of meals o Axons of ghrelin cells project to NPY, CART, POMC and AgRP circuits in ARC o Works in opposition to leptin; concentrations are inversely correlated and tightly associated with regulation of energy balance, food intake, and body mass o Plasma levels increased by stress  Leptin o predominantly produce from white adipose cells o encoded for by ob gene o ARC has highest concentration of leptin receptors o Elevated 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 o increases at the end of meals and act as satiety signals that reduce food intake o central injection increases energy expenditure o Plasma leptin expression is positively correlated with body fat mass o Leptin can increase free fatty acid oxidation and prevent storage of fat fuels in the form of triglycerides o Exogenous leptin seems to affect reproduction via indirect effects on fuel oxidation  ADH: antidiuretic hormone o Equivalent to vasopressin o released from posterior pituitary controls water uptake from collecting duct of kidney nephrons, thus has role in osmoregulation o released in response to hypovolemic thirst detected by baroreceptors in blood vessels  GOAT: ghrelin O-acyltransferase o Enzyme that activates the precursor molecule of ghrelin, allowing for ghrelin to have effect o Novel target for modulation as potential treatment of obesity, as reduction in GOAT effect reduces ghrelin and in turn reduces eating levels  MTII o MC3/4 agonist o When given to subjects, results in reduced consumption of food, as replaces the effect of a-MSH  Aldosterone o secreted by adrenal gland o controls uptake of sodium by stimulating sodium pumps in ascending limb of loop of Henle on kidney nephrons, thus has role in osmoregulation o also acts at mineralocorticoid receptors in the brain to stimulate salt appetite  Renin o Enzyme released by the kidney in response to low blood pressure o Causes the conversion of angiotensinogen to vasconstricting angiotensins  Angiotensin I, II, III o Vasoconstrictor molecules converted from angiotensinogen by renin in response to low blood pressure detected by the kidney o Act at the adrenal cortex to stimulate release of aldosterone and increase salt reuptake o Also act on the brain to stimulate drinking  CCK: Cholecystokinin o Aka bile o first gut hormone shown to affect food intake via stimulation of the vagus nerve o reduces size of ongoing meal, but not future meals o possible that some signalling occurs in the brain as well  Amylin o Hormone that is co-released with insulin o Short term effect on current food consumption, but not future meals  Glucagon o Hormone that is co-released with insulin o Short term effect on current food consumption, but not future meals o Effects mediated by the liver  Insulin o secreted by pancreas, plasma insulin level is positively correlated with body fat mass o increases at the end of meals and act as satiety signals that reduce food intake o increases energy expenditure if centrally injected o increased levels acts on hypothalamus to reduce food intake via stimulation of POMC/CART neurons of ARC  GLP-1: glucagon-like peptide 1 o peptide hormones secreted in more distal part of intestines o stimulates insulin secretion and exogenous administration decreases food intake o have more long term effects on food intake compared to CCK o possible that some signalling occurs in the brain as well  GHSR: ghrelin/growth hormone secretagogue receptor o Main receptor for ghrelin o When knocked out, stress-induced weight gain and increased caloric intake effects are eliminated, suggesting that ghrelin necessary for stress to increase these factors o Stress-induced increases in NPY and AgRP require the presence of GHSRs o Antagonists also block stress induced weight gain and increased caloric intake o Knockouts cannot defend adipose stores following stress Methods  Chronic Social Defeat Paradigm o Typically used for allowing the measurement of behavioral, endocrine and neurological variables, but with the shortcoming of applying unnatural stressors (such as foot-shocks and restraint stress) in unnatural conditions (laboratory cages rarely approximate native habitats) o Compare controls with animals who have 2 weeks of baseline measurement, 3 weeks of stress and 2 weeks of recovery o Stress increases body weight gain, total caloric intake, metabolic efficiency  Increased caloric intake attenuates the stress response by increasing ghrelin  Adrenalectomy o Removal of adrenal gland o Vastly increased salt intake when done to animals as a result of lack of aldosterone-regulated salt intake levels and dysregulation of osmoregulation  Ovariectomy o Removal of ovaries o After removal, rats increase food intake and elevates body mass 20- 25% o Knockouts (aERKO) are hyperphagic and obese o Treating ovariectomized rats with estrodial leads to hypophasia and hyperactivity o Since estrogen turns on the genes that code for progesterone receptors (PRs), PRs in fats cells are, to some extent, dependent on an anabolic effect of estrogens  Metabolic Chambers o device used for recording oxygen consumption and carbon-dioxide production for measuring metabolic activity o used to understand how metabolism works at different temperatures, especially when comparing hot versus cold blooded animals o warm blooded animals will spend more energy regulating internal temperature at non-regular temperatures, thus require increased energy to do so Brain Regions  SFO: subfornical organ o Highly vascularized region of the forebrain that does not have the BBB o Appears to play a significant role in appetite, perhaps mediated by the fact that it is the only region of the forebrain that can directly monitor peripheral blood glucose levels o Regulator of energy homeostasis  LHA: lateral hypothalamus area o Region of the hypothalamus that when lesioned results in reduced eating, and reduced motivational behaviour in general o Receives signalling from POMC, CART, NPY and AgRP neurons o NPY signalling results in release of body mass regulatory molecules orexin and MCH in LHA  VMH: ventromedial hypothalamus o lesions supress sympathetic nervous system activity and increase parasympathetic nervous system activity resulting in increased fat storage while inhibiting lipolysis  PVN: paraventricular nucleus of hypothalamus o Primary location affected by the feeding excitatory and inhibitory circuits o Contains receptors for NPY, a-MSH (MC4), CART and AgRP o Magn
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