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Systems Neurophysiology- BMSC3139 > Central control of food intake > Flashcards

Central control of food intake Flashcards

1
Q

What are of the brain is involved in controlling food intake ?

A

hypothalamic arcuate nucleus neurones

  • stimulate and inhibit food intake for long term energy balance
  • very small nucleus yet it has such a great influence
  • it can also induce quite rapid actions
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2
Q

How is the brainstem involved in controlling food intake ?

A

signals act on vagal afferents to tell you when your are hungry or full

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3
Q

Where are the vagal afferents receiving info from in the control of food intake ?

A

from the gut
through nutrient receptors which are chemoreceptors that can respond to hormones
also from stretch receptors

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4
Q

What is leptin ?

A

it is a hormone released from fat cells and it acts upon the hypothalamus
it increases satiety- reduces food intake

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5
Q

What is gherlin ?

A

it is a hormone released from the GIT, and its secreted when the stomach is empty to increase hunger and food intake

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6
Q

What is insulin ?

A

it is a hormone released from the pancreas

it increases satiety and suppresses eating

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7
Q

What does leptin do ?

A

it circulates in proportion to body fat stores
it enters the brain in proportion to its plasma level
inhibits AgRP neurones
stimulates POMC cells
excites vagal afferents
inhibits food intake

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8
Q

What is wrong with the fat mouse and what does it show?

A

it has no leptin or it lacks the leptin receptors
it shows that there are mechanisms that can control eating in a homeostatic fashion - demonstrate there is an automatic stopping to eating

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9
Q

What does gherlin do ?

A

stimulates food intake
increases adiposity
has receptors on some of the same brain cells as leptin receptors in arcuate nucleus
stimulates AgRP

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10
Q

What method has been used to help elucidate the pathways involved in food intake ?

A

it has been deciphered by optogenetics

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11
Q

What happens when POMC cells are stimulated ?

A

decrease food intake and increase energy expenditure so leptin stimulates these

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12
Q

What happens when the AgRP neurones are stimulated ?

A

increases food intake and it can also cause inhibition of POMC cells

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13
Q

What happens to mice that have their AgRP neurones activated ?

A

they will eat even if they are full, they just continue to eat

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14
Q

What happens when ChR2 is expressed in AgRP neurones ?

A

stimulation of these cells causes a voracious food intake even through these mice were already well fed
they started eating within 6 mins of stimulation

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15
Q

What is chemogenetics?

A

it is when you cause the expression of a designer receptor which can be activated by a drug that doesn’t resemble anything else in the body
enables you like optogenetics to induce a specific effect

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16
Q

What chemogenetic experiments were carried out in food intake control ?

A

expresssed excitatory DREADD receptor in AgRP neurones
they then stimulated this receptor with a complimentary agonist, CNO
they took slices to record the electrical activity
within a couple of mins after CNO application the ap firing rates had increased and it was maintained

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17
Q

What experiment was used to prove DREADD worked in vivo?

A

when CNO was injected intraperitonally it activated DREADD expressing cells
these cells had a massive increase in c-fos demonstrating increased cell activity

18
Q

What did a single injection of CNO cause?

A

increases food intake for several hours

19
Q

What did daily injections of CNO cause?

A

the mice put on a lot of weight

in 5days they had gone from 24g to 28g

20
Q

What was interesting when they stopped the daily CNO injections to the mice ?

A

the mice didn’t maintain the excessive body weight - they went back to their normal weight, suggesting that in the CNS there is a set point for an appropriate body weight

21
Q

What happened when an inhibitory DREADD was expressed in AgRP neurones ?

A

it hyperpolarises the AgRP neurones and therefore it decreases food intake

22
Q

What does leptin do to AgRP neurones ?

A

inhibits AgRP neurones
leptin hyper polarises the hypothalamic glucose responsive neurones which are the AgRP neuters
it also increases input resistance making the cells less excitable

23
Q

What does tolbutamide do to AgRP neurones?

A

it is a blocker of some potassium channels and it reduces some of the effects of leptin but doesn’t completely abolish them

24
Q

What does gherlin do to AgRP neurones?

A

using a loose cell attached patch recordings it showed that it increases the firing rates of these neurones

25
Q

What happened when ChR2 was expressed in POMC cells?

A

stimulation inhibits eating and results in decreased body weight

26
Q

What hormone excites POMC cells?

A

leptin

cells are excited by leptin for a while after leptin has been applied

27
Q

What effect does gherlin have on POMC neurones?

A

causes about 50% decrease in spontaneous activity

it maintains their neurones at a reduced firing rate for a while

28
Q

What effects do AgRP neurones?

A

inhibit POMC cells
the AgRP neurones contained ChR2 and they were activated whilst recording activity from POMC cells
the activity recorded in the POMC cells was IPSCs - they could block this inhibitory effect with a blocker of excitatory aa transmission showing that these post synaptic currents are mediated by GABA currents

29
Q

When they looked at the connections between neurones involved in food intake, what was seen ?

A

only really appeared to be a connection from the AgRP neurones to the POMC neurones and its connections were strong - 90%
POMC cells can be completely inhibited by AgRP neurones -profound effect

30
Q

What happened when both AgRP and POMC expressed ChR2?

A

they were both activated but even though activation of POMC normally inhibits food intake there was still an increase in food intake indicating that the AgRP neurones have another way of stimulating food intake

31
Q

What happens to AgRP neurones when they are activated in the PVH?

A

increases food intake
AgRP neurones express ChR2 and this is also expressed in their terminals so if food intake is increased by stimulating the PVH then their terminals must be present in the PVH
this shows that the AgRP neurones also project to the PVH

32
Q

What happens to the AgRP neurones when the PBN is activated?

A

it didn’t cause an increase in food intake

33
Q

What effect do AgRP neurones have on PVH neurones?

A

inhibits these neurones
this inhibition can be blocked by GABA antagonist picrotoxin
burst stimualtion causes pronlonged inhibition of the PVH cells

34
Q

How did they put an inhibitory DREADD into PVH neurones and what happened?

A

put the inhibitory DREADD under the control of the sim1 promoter
when these cells were activated causing their inhibition it caused an increase in food intake
this is consistent with AgRP cells acting to inhibit the PVH cells

35
Q

What does direct activation of PVH cells cause?

A

activation of both AgRP and PVH- PVH activated directly by optogenetics
this can override the AgRP inhibition of the PVH cells and this prevents increased food intake which normally occurs when the AgRP is activated

36
Q

What happened when both AgRP and oxytocin cells of PVH are activated?

A

the oxytocin cells in the PVH can override the inhibition induced by AgRP neurones
therefore overriding food intake

37
Q

What happens to the increased food intake induced by AgRP activation, when NPY-Y1R and GABAAR antagonists are applied?

A

food intake is reduced by both antagonists when the AgRP neurones are stimulated by the PVH

38
Q

What did DREADD stimualtion and application of antagonists prove?

A

applying DREADD stimulation causes activation all outputs and this was still reduced by these antagonists but it was still above baseline so PVH is not the only important site for AgRP effects

39
Q

What is prader-willi syndrome?

A

it is caused by sim1 mutations
causes loss of function in oxytocin neurones in PVH
causing overeatinf and obesity

40
Q

What surprising effect was found in the PVH?

A

PVH stimulation is anorexigenic - also contains cells that increase food intake
these cells contain glutamate
when these cells were excited they elicited epscs in AgRP cells

41
Q

What cell types in the PVH excited AgRP neurones ?

A

pvh cells expressing TRH and PACAP but not pro-dynorphin
these cells project to the AgRP neurones
they dont excite POMC cells
AgRP cells dont excite the TRH pvh cells

42
Q

What happened when an excitatory DREADD was expressed in TRH or PACAP PVH cells?

A

it caused animals to eat more as it drives AgRP neurones

Systems Neurophysiology- BMSC3139 (11 decks)

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