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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
how does LLC tumor cell implantation affect cgrp neurons in pbn
increases cgrp neuron activity
26
effect of inhibiting cgrp neurons in pbn in cancer + conclusion drawn
protects against cancer-mediated weight loss and anorexia -> cancer acts via cgrp to decrease body weight
27
role of cgrp neurons in pbn in normal body weight or energy
not required
28
relationship bw gdf-15 and cgrp neurons in pbn
gdf-15 activates cgrp neurons in pbn
29
relationship bw gfral neurons in ap and cgrp neurons in pbn
activating gfral neurons activates cgrp neurons (projections from AP -> PBN)
30
effect of silencing cgrp neurons in pbn on effects of gdf-15
stops the aversive and anoretic properties of gdf-15 (normal aversion, no anorexia)
31
effect of activating PBN -> CeA circuit (2)
aversion to saccharine water and reduction in food intake
32
inject virus in pbn, effect of shining blue light (for Ch2R) in (a) CeA (b) BNST (c) VPMpc
(a) aversion + decreased food intake (b) aversion + decreased food intake (c) no aversion + no effect on food intake
33
which neurons does gdf-15 activate in central amygdala
PKCδ
34
effect of activating PKCd neurons (2)
1. reduction in food intake 2. aversion
35
how do pathogenic states act through CNS to suppress feeding (7)
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
anoretic and aversive properties of gdf-15 are dependent on what
cgrp pbn neurons
37
brainstem receives input from (3)
1. gut 2. pancreas 3. adipose tissue (leptin)
38
basics of gut-brain signaling (3)
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
where does nodose project to (2)
1. gut (stomach and intestine) 2. brainstem (AP/NTS)
40
specificity of EEC classes
most classes express sensors for several things
41
what do EECs express
macronutrient sensors
42
effect of activating EECs
reduction of food intake
43
what are cck neurons and what signal do they convey
EECs; signal satiety
44
how test that activating EECs is reinforcing + result of test and why
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
location of nodose neurons
next to trachea
46
ND neurons respond to (2)
1. distention (stretch) 2. nutrients
47
which ND neurons respond to food and stretch in (a) stomach, (b) intestine
(a) same ND neurons respond to both (b) different ND neurons respond to respective stimulus
48
what technique was used to test which ND neurons project where in gut + result
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
what type of neuron are ND neurons
bipolar cells
50
the response of NTS to nutrients relies on what + what did they do to discover that
vagus nerve; severed vagus nerve -> attenuation of sugar and fat-mediated activation of NTS neurons
51
which brain areas (and which neurons) do ND neurons communicate with (6)
1. AP - brainstem 2. NTS - brainstem 3. PVH - hypothalamus 4. PBNdl 5. DA neurons in VTA - midbrain 6. DA neurons in SNc - midbrain
52
effect of stimulating NTS projections (Ch2R) from ND (light in NTS; virus in ND)
decreased food intake
53
effect of infusing nutrients into the stomach on agrp neuron activity
reduction of agrp neuron activity
54
how test relationship bw NTS projections from ND neurons and reward (DA)
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
secretion of amylin (2)
1. produced by beta cells in pancreas 2. co-secreted with insulin following meal
56
what receptor does amylin bind to and where is it expressed
calcitonin receptor; AP/NTS
57
effect of calcitonin receptor agonist in AP/NTS neurons
activates them (increased FOS)
58
effect of activating NTS calcr neurons (2)
1. reduced food intake 2. reduced body weight
59
activation of NTS or AP calcr neurons and aversion
following the CTA assay, mice don't avoid saccharose water -> calcr neurons don't have aversive properties
60
neurocircuitry of NTS calcr neurons vs NTS cck cells
1. both project to PBN 2. only calcr neurons project to PVH/hypothalamus
61
where is leptin receptor expressed
NTS
62
effect of activating NTS LepR (2)
1. reduced food intake 2. reduced body weight
63
therapies targeting brainstem neurons (4)
1. amylin analogs 2. gdf-15/gfral based therapies 3. glp1 receptor agonists 4. glp1-gip dual agonists
64
effects of amylin agonist, pramlintide (2)
1. reduction in body weight 2. no nausea
65
effect of NTS calcr-KO
stops davalintide-mediated anorexia (amylin agonist) -> no decreased body weight or food intake
66
effect of gdf-15 antagonists (3)
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
what do glp1 cells sense
glucose and fat
68
which tissues does glp1 act on
multiple tissues: brain, pancreas, kidney, muscle, bone, heart, GIT, liver
69
effect of glp1-r agonists
decrease body weight in obese humans
70
where are glp1-r expressing neurons expressed
widely across cns
71
what does exogenous glp1 activate and where
glp1-r expressing neurons in ap
72
what do ap glp1-r encode
aversive properties of glp1 receptor agonists
73
effect of restoring glp1-r only in ap
restores aversive properties of glp1 agonist (sufficient)
74
effect of deleting glp1-r only in ap
stops aversive properties of glp1 agonists (necessary)
75
effect of glp1-gip dual agonist
reduces body weight in obese patients
76
where are gip-r expressed
within ap
77
brain area most successful anti-obesity therapeutics target
brainstem

anat 322 (7 decks)

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