Hypothalamic Control Food Intake #2:neural Plasticity

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leptin responsible for (2)

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controlling body weight and reproduction

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in a leptin deficient ob/ob mice they are

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obese and infertile

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obese women and lean women are ______ because______

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infertile because starvation leads to decreased gonadal hormones and delays ovulation.

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its not the change in body weight that affects infertility but

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impairment of leptin signaling

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explain reproductive control by CNS

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leptin affects reproductive axis by activating GnRH neurons. The GnRH neurons have no leptin receptor so hypothesis is that other neurons with leptin receptors project to GnRH neurons Orexigenic

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orexigenic and an example

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drug or neuropeptide hormone that increases appetite ie appetite stimulant ex)ghrelin

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anorexigenic and an example

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reduces appetite ie appetite suppressant ex)leptin

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anorexigenic and orexigenic are

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cns modulators of food intake

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in the arcuate nucleus have POMC which____onto MC3/4R(PVN) and NPY/AgRP which ___onto MC3/4R
leptin stimulates ____ and inhibits _____. Ghrelin stimulates ____

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decreases food intake;increase food intake;POMC;NPY/AgRP;NPY/AgRP

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only orexigenic gut hormone

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ghrelin

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ghrelin has two activities

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appetite stimulating,growth hormone releasing

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ghrelin receptor

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GHSR: growth hormone secretagogue receptor

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cells making ghrelin found in gi tract in high concentration

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at the bottom of the stomach

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ghrelin plays role in meal initiation because

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ghrelin in plasma increases during fasting/before a meal and falls after an hour after meal

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after diet induced weight loss plasma levels of ghrelin

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increase a lot may be reason for rebound weight gain

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gastric bypass surgery

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suppresses ghrelin levels

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in an experiment where cancer patients with impaired appetite, they were given ghrelin which

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increased energy intake

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CCK made in (2)

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made in gut and CNS

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receptors CCK-1 and CCK-2 where is each found more in

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CCK-1: GI tract
CCK-2: CNS

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release of CCK form intestines occurs due to _____specifically ___&__ in the chyme

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nutrient stimulation;fats;proteins

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shown by Gibbs at cornell that exogenous cck in rats caused

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decreased meal size. CCK is an anorexogenic. this experiment also done in humans

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cck needs to be administered when to affect meal size

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less than 15min

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is cck effective for long term wight loss

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no because its seen in rats tha chronic cck usage doesnt affect weight loss because animals just eat more freq to compensate

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lorglumide

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CCK receptor antagonist

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CCK interacts with

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leptin

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both lorglumide and leptin together

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increases food intake but when no loglurmide and just leptin get food intake increase

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proglucagon made by ______and when modified posttranslationally get ____

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enteroendocrine cells of intestines; GLP-1 (glucagon like peptide 1)

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release of GLP-1 due to

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nutrient stimualtion by fats or carbs

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GLP-1 is an ____

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incretin

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incretins

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gastrointestinal hormone that increase insulin secretion without increasing blood glucose levels. Does this during meals

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GLP-1 receptor found in periphery (2) and widespread throughout ____

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endocrine pancreas/gut;CNS

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in like 2min GLP-1 degraded by

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dipeptidyl peptidase IV (DPP-I)

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peripheral injection of GLP-1 agonist in rats caused

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decrease in food intake and cause wight loss

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why is GLP-1 good canidate to treat obesity/type 2 diabetes

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reduces food intake and stimulates insulin secretion

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since GLP-1 broken down so quick in treatments they use

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exendin -4

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exendin -4

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-isolated from Gila moster venom
-agonist of GLP-1 receptor
-greater half life than GLP-1
-treat obesity/diabetes

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placing GLP-1 antagonist by intracerebroventricular infusion caused (2)

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increase food intake & obesity

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OXM (4)

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-anorexogenic
-found on same preproglucagon gene that GLP-1 comes form
-also released due to fats or carbs
-inhibits food intake when given to rodents and suppresses appetite in humans(so less energy intake after meal)

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seen that with OXM injection before meals (preprandial) chronically caused

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weight loss in obese patients

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Peptide YY(PYY) (7)

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-made in eneteroendocrine cells in ileum/colon
-secreted after meal to delay gastric emptying
-tyrosine at either end of peptide
-in brain it binds to presynaptic Y2 receptos in hypothalamus and inhibits NPY neurons and depresses feeding
-anorectic effect in rodent controversial
-in nonhuman primates intramuscular injection show reduced food intake
-in humans intravenous injections reduce caloric intake in normal and obese people

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brain plasticity is made up of (4)

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synaptic strengthening, synaptic elimination/weaking, synaptogensis&synapse remodeling, neurogenesis

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synaptic strengthening

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occurs during learning, memories are stabilized and stored as modifications of synaptic strength within existing neuronal circuits

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synaptic elimination/weakening

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mechanism for forgetting, may serve to weaken unused connections that could be advantage for info storage

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synaptogenesis and synaptic remodeling

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in adult, synaptogenesis seen in response to denervation, suggests that sprouting of axon collaterals and growth of new synapses to occupy vacated sites

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neurogenesis

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new neurons continue to be added to adult brain throughout life

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barrel cortex

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dark staining region of layer four in somatosensory cortex where info from contralateral side comes from thalamus. Study it to understand plasticity like dendritic spines in vivo
-involves whiskers

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astrocytic processes in SON show

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plasticity

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astrocytic processes between SON neurons and around axonal terminals are unstimulated in virgins/postweaned rats and stimulated like in lactating rats see

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retraction of processes which favors diffusion of released glutamate in EX space which can then act on adjacent synapses (intersynaptic cross talk interactions)

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theres link between hypothalamic plasticity and (2)

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reproduction and energy homeostasis

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leptin deficient mice differ from normal in that

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theres different number of excitatory and inhibitory inputs onto NPY and POMC neurons.

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when leptin given to ob/ob mice synaptic density

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rapidly normalized

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Dil

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fluorescent lipophilic dye that labels axonal projections

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leptin deficiency disrupts

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projections from arc to PVN

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leptin promotes neurite ___from __

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outgrowth;arc nucleus

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leptin on hypothalamus does three things

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Leptin acts directly on the neurons of the arcuate nucleus by binding to the leptin receptors, which results in
changes in their production and release of the neuropeptide NPY and the POMC product, α-melanocyte
stimulating hormone.
-Leptin produces rapid changes in the strength and number of excitatory and inhibitory synapses that have
inputs on NPY and POMC arcuate neurons.
-Leptin induces neurite outgrowth of arcuate neurons, stimulating projections from the arcuate to the
paraventricular nucleus (PVN) of the hypothalamus during a critical postnatal period.

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molecular basis of leptin mediated plasticity in brain remains

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elusive

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DIO rats (diet induced obesity) are known to be

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leptin resistant before they become obese

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use DIO rats to

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see hypothalamic plasticity

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in DIO rats the arc nucleus response to leptin is

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reduced ie DIO rats arc projections are defective

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is obesity predisposed in brain

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yes possibly

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Ciliary Neurotrophic Factor (CNTF) induces

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induces sustained weight loss in obese subjects.

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bromo-­‐deoxyuridine (BrdU=)

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marker for DNA synthesis

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HU

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neuron specific RNA binding protein

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APC

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oligiodendrocyte marker

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some new born hypothalamic cells are responsive to ___use ___&___ colabeling

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leptin;BrdU/pSTAT3

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CNTF induces

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cell proliferation in murine hypo

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many new born cells appear to be committed to

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neuronal fate

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is there a causal link between CNTF action and hypo neurogenesis

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...

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Ara-C

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inhibits cell proliferation,it acts as competitive inhibitor of DNA polymerase

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Brdu+CNTF shows decline in body weight but Brdu+CNTF+AraC

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shows sharper decline after surgery but shoots back up

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mitotic blockade=

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AraC treatment
-abolishes the long term but not the short term effect of CNTF on weight

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CNTF induced neurogenesis contributes to

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sustained CNTF dependent weight loss

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Leptin provides a key feedback signal from
peripheral adipose to two types of neurons in the
arcuate nucleus of the hypothalamus. POMC
neurons (brown) are activated by leptin and inhibit
food intake and increase energy expenditure,
whereas AgRP/NPY neurons (blue) have the
opposite response to leptin and the opposite effect
on energy balance.

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..

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before CNTF is administered

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body fat has
expanded because the key central nervous system
targets of leptin are less responsive.

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during CNTF treatment

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body weight is lowered
because CNTF mimics leptin effects in the
hypothalamus. In addition, CNTF treatment
stimulates the formation of new neurons (orange)
involved in weight regulation.

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after CNTF treatment

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these new neurons increase
the effects of leptin and thereby keep adipose mass
from returning to its previous levels.