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anat 322 > brainstem control of appetite > Flashcards

brainstem control of appetite Flashcards

1
Q

what does the NTS control (5)

A
  1. food intake
  2. HR
  3. breathing
  4. taste
  5. reflexes (gag, vomit)
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2
Q

feeding pathways through NTS (2)

A
  1. pathology-related appetite suppression (emergency system)
  2. relaying physiologic anoretic cues
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3
Q

how weight loss affects mortality rate in cancer patients

A

weight loss predicts greater mortality in cancer

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4
Q

diseases weight loss is clinically relevant in (2)

A
  1. cancer
  2. COPD
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5
Q

what is GDF-15

A

factor secreted by tumors (circulating levels are increased in cancer patients)

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6
Q

instances when GDF-15 is increased (4)

A
  1. bacterial and/or viral infection
  2. hepatic fibrosis
  3. food poisoning (mycotoxin)
  4. cancer
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7
Q

oxygen levels in tumor microenvironment

A
  1. normal O2 level near blood vessels
  2. hypoxia (low O2) at core of tumor
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8
Q

how does hypoxia influence GDF-15

A

increases GDF-15 mRNA and protein levels via ER stress-dependent pathway (ER stress = increased GDF-15 expression)

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9
Q

ER stress DIRECTLY increases levels of which protein

A

CHOP

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10
Q

relationship bw CHOP and GDF-15

A

CHOP drives GDF-15 expression in states of ER stress and hypoxia (CHOP-KO = decreased GDF-15 expression)

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11
Q

effect of exogenous GDF-15 administration (5)

A
  1. reduction of food intake
  2. reduction in body weight
  3. aversion
  4. nausea
  5. emesis
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12
Q

how test that GDF-15 induces aversion/nausea

A

conditioned taste avoidance/aversion (CTA) assay
1. conditioning: expose animal to saccharine-flavored water and drug treatment (simultaneously)
2. testing: without drug treatment, animal chooses bw saccharine water and normal water

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13
Q

results of the CTA assay and why

A

animals preferred normal water (instead of usual saccharine water) because now associate drug with saccharine water: drug induces nausea and animal doesn’t want that feeling, so avoids the saccharine water (associated with nausea)

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14
Q

effect of GDF-15 overexpression in non-cachetic tumor cell line

A

reduces body weight (even when non-cachetic tumor cells normally don’t)

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15
Q

GDF-15 levels and clinical outcomes

A

elevated GDF-15 levels associated with worsened clinical outcomes

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16
Q

which receptor does GDF-15 act through to decrease body weight

A

GFRAL

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17
Q

where is gfral expressed

A

ap and nts only (not other feeding centers)

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18
Q

role of gdf-15 and gfral in normal energy and body weight

A

not needed for normal energy balance or body weight (non-cancer)

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19
Q

location of gfral terminals

A

mostly ap, some in nts (viewed with gfral Cre-ER)

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20
Q

brain area where ap gfral neurons project and NOT project to

A

project to parabrachial nucleus; don’t project to hypothalamus

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21
Q

specific compartment of PBN that gfral ap neurons terminate in

A

external lateral compartment of the pbn (elPBN)

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22
Q

what kind of neuron are cgrp neurons and what do they express

A

population of elPBN neurons (express cgrp peptide)

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23
Q

effect of activating cgrp neurons in pbn (3)

A
  1. reduces body weight
  2. reduces food intake
  3. promotes aversive behaviors (avoiding sucrose water)
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24
Q

what activates cgrp neurons in the pbn

A

pathogenic states; LiCl (irritant) or LPS (mimics infection); cancer (tumors -> GDF-15)

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25
Q

how does LLC tumor cell implantation affect cgrp neurons in pbn

A

increases cgrp neuron activity

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26
Q

effect of inhibiting cgrp neurons in pbn in cancer + conclusion drawn

A

protects against cancer-mediated weight loss and anorexia -> cancer acts via cgrp to decrease body weight

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27
Q

role of cgrp neurons in pbn in normal body weight or energy

A

not required

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28
Q

relationship bw gdf-15 and cgrp neurons in pbn

A

gdf-15 activates cgrp neurons in pbn

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29
Q

relationship bw gfral neurons in ap and cgrp neurons in pbn

A

activating gfral neurons activates cgrp neurons (projections from AP -> PBN)

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30
Q

effect of silencing cgrp neurons in pbn on effects of gdf-15

A

stops the aversive and anoretic properties of gdf-15 (normal aversion, no anorexia)

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31
Q

effect of activating PBN -> CeA circuit (2)

A

aversion to saccharine water and reduction in food intake

32
Q

inject virus in pbn, effect of shining blue light (for Ch2R) in (a) CeA (b) BNST (c) VPMpc

A

(a) aversion + decreased food intake
(b) aversion + decreased food intake
(c) no aversion + no effect on food intake

33
Q

which neurons does gdf-15 activate in central amygdala

A

PKCδ

34
Q

effect of activating PKCd neurons (2)

A
  1. reduction in food intake
  2. aversion
35
Q

how do pathogenic states act through CNS to suppress feeding (7)

A
  1. hypoxia in tumor microenvironment
  2. increased CHOP (ER stress)
  3. increased GDF-15
  4. activation of AP/NTS GFRAL neurons
  5. activation of CGRP neurons in PBN
  6. activation of PKCδ neurons in CeA
  7. reduced appetite & visceral malaise
36
Q

anoretic and aversive properties of gdf-15 are dependent on what

A

cgrp pbn neurons

37
Q

brainstem receives input from (3)

A
  1. gut
  2. pancreas
  3. adipose tissue (leptin)
38
Q

basics of gut-brain signaling (3)

A
  1. mechanosensors signal lumen distension after meal
  2. enteroendocrine cells (EECs) signal meal composition after meal
  3. both signals communicated via the nodose (ND) to CNS
39
Q

where does nodose project to (2)

A
  1. gut (stomach and intestine)
  2. brainstem (AP/NTS)
40
Q

specificity of EEC classes

A

most classes express sensors for several things

41
Q

what do EECs express

A

macronutrient sensors

42
Q

effect of activating EECs

A

reduction of food intake

43
Q

what are cck neurons and what signal do they convey

A

EECs; signal satiety

44
Q

how test that activating EECs is reinforcing + result of test and why

A
  1. baseline: expose mouse (CCK-Cre) to 2 flavors
  2. training: mix CNO with flavor B (create association)
  3. test: which flavor does mouse prefer
    result -> prefer flavor with CNO
    why -> with CNO, CCK cells are activated. can infer that prefer this state because it decreases appetite, which is a good feeling -> activating EECs (CCK) = good feeling/reinforcing
45
Q

location of nodose neurons

A

next to trachea

46
Q

ND neurons respond to (2)

A
  1. distention (stretch)
  2. nutrients
47
Q

which ND neurons respond to food and stretch in (a) stomach, (b) intestine

A

(a) same ND neurons respond to both
(b) different ND neurons respond to respective stimulus

48
Q

what technique was used to test which ND neurons project where in gut + result

A
  1. purple retrograde tracer injected into stomach
  2. green retrograde tracer injected into intestine
  3. if overlap -> same ND neuron projects to both stomach and intestine
  4. if no overlap -> distinct ND neurons project to stomach vs intestine
    result: no overlap = one-to-one projection
49
Q

what type of neuron are ND neurons

A

bipolar cells

50
Q

the response of NTS to nutrients relies on what + what did they do to discover that

A

vagus nerve; severed vagus nerve -> attenuation of sugar and fat-mediated activation of NTS neurons

51
Q

which brain areas (and which neurons) do ND neurons communicate with (6)

A
  1. AP - brainstem
  2. NTS - brainstem
  3. PVH - hypothalamus
  4. PBNdl
  5. DA neurons in VTA - midbrain
  6. DA neurons in SNc - midbrain
52
Q

effect of stimulating NTS projections (Ch2R) from ND (light in NTS; virus in ND)

A

decreased food intake

53
Q

effect of infusing nutrients into the stomach on agrp neuron activity

A

reduction of agrp neuron activity

54
Q

how test relationship bw NTS projections from ND neurons and reward (DA)

A
  1. self-stimulation DA task
  2. laser stimulates NTS terminals from ND neurons
  3. when laser active, increase button pokes because activating laser (ND neurons) causes release of DA
  4. DA is rewarding so learn that active laser (ND neurons) = reward
55
Q

secretion of amylin (2)

A
  1. produced by beta cells in pancreas
  2. co-secreted with insulin following meal
56
Q

what receptor does amylin bind to and where is it expressed

A

calcitonin receptor; AP/NTS

57
Q

effect of calcitonin receptor agonist in AP/NTS neurons

A

activates them (increased FOS)

58
Q

effect of activating NTS calcr neurons (2)

A
  1. reduced food intake
  2. reduced body weight
59
Q

activation of NTS or AP calcr neurons and aversion

A

following the CTA assay, mice don’t avoid saccharose water -> calcr neurons don’t have aversive properties

60
Q

neurocircuitry of NTS calcr neurons vs NTS cck cells

A
  1. both project to PBN
  2. only calcr neurons project to PVH/hypothalamus
61
Q

where is leptin receptor expressed

A

NTS

62
Q

effect of activating NTS LepR (2)

A
  1. reduced food intake
  2. reduced body weight
63
Q

therapies targeting brainstem neurons (4)

A
  1. amylin analogs
  2. gdf-15/gfral based therapies
  3. glp1 receptor agonists
  4. glp1-gip dual agonists
64
Q

effects of amylin agonist, pramlintide (2)

A
  1. reduction in body weight
  2. no nausea
65
Q

effect of NTS calcr-KO

A

stops davalintide-mediated anorexia (amylin agonist) -> no decreased body weight or food intake

66
Q

effect of gdf-15 antagonists (3)

A
  1. ameliorates weight loss mediated by cancer and cisplatin (cancer treatment)
  2. ameliorates anorexia and emesis (induced by cisplatin)
  3. increased survival in a mouse cancer +/- chemotherapy model
67
Q

what do glp1 cells sense

A

glucose and fat

68
Q

which tissues does glp1 act on

A

multiple tissues: brain, pancreas, kidney, muscle, bone, heart, GIT, liver

69
Q

effect of glp1-r agonists

A

decrease body weight in obese humans

70
Q

where are glp1-r expressing neurons expressed

A

widely across cns

71
Q

what does exogenous glp1 activate and where

A

glp1-r expressing neurons in ap

72
Q

what do ap glp1-r encode

A

aversive properties of glp1 receptor agonists

73
Q

effect of restoring glp1-r only in ap

A

restores aversive properties of glp1 agonist (sufficient)

74
Q

effect of deleting glp1-r only in ap

A

stops aversive properties of glp1 agonists (necessary)

75
Q

effect of glp1-gip dual agonist

A

reduces body weight in obese patients

76
Q

where are gip-r expressed

A

within ap

77
Q

brain area most successful anti-obesity therapeutics target

A

brainstem

anat 322 (7 decks)

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