Neural control of motivational behaviour Flashcards

1
Q

what characterises areas called circumventricular organs? [1]

give some e.g.s xx

A

what characterises areas called circumventricular organs? [1]
areas where BBB is leaky, capillaires have fenestrations & substances can come in like hormone

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2
Q

which regions of the brain detect whether you are thirsty? [2]
- which ventricle are they close to? [1]

A

which regions of the brain detect whether you are thirsty? [2]
subfornical
OVLT

- which ventricle are they close to? [1]
third ventricle

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3
Q

the part of the brain that detects thirst is close to

corpus callosum
lateral ventricles
third ventricles
fourth ventricles
cerebral aqauduct

A

the part of the brain that detects thirst is close to

corpus callosum
lateral ventricles
third ventricles: OVLT & subfornical glands are located near
fourth ventricles
cerebral aqauduct

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4
Q

which of the following detects changes in osmolality?

median eminence
posterior pituitary
subcommissural organ
pineal gland
subfornical organ

A

which of the following detects changes in osmolality?

median eminence
posterior pituitary
subcommissural organ
pineal gland
subfornical organ & OVLT: contain osmoreceptors !

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5
Q

hypertonic blood is detected in the subfornical organ & OVLT (in wall of 3rd ventricle).

which nucleus do ^ activate when this occur? what does this cause to happen? [3]

A
  • activates cells in mediate preoptic nucleus of hypothalamus
  • projects to limbic system to drink & regulate thirst - we seek out water (greater activity = more thirsty)

ALSO

  • subfornical organ activates cell in paraventricular nucleus & supraoptic nucleus: release ADH from posterior pit.
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6
Q

which nuclei are stimulated when blood is hypertonic? [3]

A
  • medial preoptic nuclei
  • paraventricular nuclei
  • supraoptic nuclei
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7
Q

what are the three effects of ADH to decrease loss of water ? [3]

A
  • increase aquaporins in CD
  • increases perm. of urea in CD (helps increase reab)
  • stimulates Na reaborb by increase Na/K/Cl2 transporter
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8
Q

what happens to body when in heat stress?

A
  • lose water by sweat
  • drink more to compensate
  • body increase aldosterone (to replace Na+ lost)
  • decreases ANP

= prevents hyponatramia

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9
Q

there is a delay between fluid intake alteration of plasma osmlality (10/20mins), but you feel not thirsty immediately after having a drink. how does this occur?

A

neural input to the brain from oropharnx that signals fluid intake (vagal afferents)
ADH release immediately inhibited

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10
Q

what happens to u if litro no water available in the desert lol?

A

conflict between water conservation and temp regulation:

  • initially sweating continues, but body temp rises a few degrees
  • urine flow stops completely
  • become so dehydrated, cant sweat. over heat & get heat stroke and death
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11
Q

where is the main storage of energy in body? [1]

what happens to body weight and fat, despite fluctuations in food intake? [1] name? [1]

A

where is the main storage of energy in body? [1]
adipose tissue

what happens to body weight and fat, despite fluctuations in food intake? [1]
stays the same

name? [1]
**adipostatic model

baso controls feeding and maintains weight**

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12
Q

which part of the brain has the satiety centre?

thalamus
pituitary gland
cerebellum
hypothalamus
medulla

A

which part of the brain has the satiety centre?

thalamus
pituitary gland
cerebellum
hypothalamus
​medulla

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13
Q

in rat studies:

lesions in the lateral hypothalamus produced which condition? [1]

lesions in the media hypothalamus produced which condition? [1]
specicially which medial nuclei? ^ [2]

A

in rat studies:

lesions in the lateral hypothalamus produced which condition: anorexia

​lesions in the media hypothalamus produced which condition: **obesity

  • arcuate nucleus
  • periventricular nucleus**
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14
Q

hunger is a balance of internal and external cues. what are these?

A

internal cues:

  • contraction of stomach
  • glucose, insulin, ghrelin, CCK & leptin levels

external cues:
- sight and smell of food

BALANCE OF THE TWO controls hunger

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15
Q

which of the following is where internal cues (such as blood hormones are detected) when controlling hunger?

lateral hypthalamic nucleus
arcuate nucleus
periventricular nucleus
supraoptic nucleus
paraventricular nucleus

A

which of the following is where internal cues (such as blood hormones are detected) when controlling hunger?

lateral hypthalamic nucleus
arcuate nucleus
periventricular nucleus
supraoptic nucleus
paraventricular nucleus

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16
Q

lesions in which part of brain cause inability to detect internal signals? [1]

A

arcuate nucleus

17
Q

which cell types in the arcuate nucleus

a) increase hunger? [2]
b) decreaes hunger? [2]

A

grehlin / insulin & other hormones travel to arcuate nucleus and interact with some cell types:

increase hunger:

  • Agouti-related peptitde (AGRP)
  • neuropeptide Y neurones (NPY)

decrease hunger

  • cocaine & amphethamine transcript neurones (CART)
  • pro-opiomelanocortin (POMC)

& interact !!

18
Q

which of the following hormones is the hunger hormone?

leptin
insulin
ghrelin
neuropeptide Y
CCK

A

which of the following hormones is the hunger hormone?

leptin
insulin
ghrelin
neuropeptide Y
CCK

19
Q

ghrelin is mainly released from which part of the stomach? [1]

which nerve detects stomach contractions & causes release of ghrelin? [1]

ghrelin causes the release of which hormones from arcuate nucleus? [2]

A

ghrelin is mainly released from which part of the stomach? [1]
fundus (but also pancreas & ileum)

which nerve detects stomach contractions & causes release of ghrelin? [1]
vagus nerve detects stomach contractions and signals to brainstem & hypothalamus to release ghrelin

ghrelin causes the release of which hormones from arcuate nucleus? [2]
neuropeptide Y
agouti related peptide

20
Q

what does ghrelin cause the release of ? [3] & inhibit [2] in arcuate nucleus

A

ghrelin in the arcuate nucleus

  • stimualtes
    i) agouti-related peptide (AGRP) & neuropeptide Y (NPY): mediate hunger sensation
    ii) dopamine pathway when eating
  • inhibits POMC & CART: satiety signalling
21
Q

where is cholecystokinin released from?

pancreas
stomach
small intestine
bile duct
oesphogus

A

where is cholecystokinin released from?

pancreas
stomach
small intestine
bile duct
oesphogus

22
Q

what it the role of CCK? [2]

where does it travel after release from small intestine? [1]

A

what it the role of CCK? [1]
release of digestive enzymes from pancreas
produces satiety !!

where does it travel after release from small intestine? [1]
arcuate nucleus in hypothalamus

23
Q

which hormone causes nausea?

insulin
ghrelin
leptin
GLP-1
CCK

A

which hormone causes nausea?

insulin
ghrelin
leptin
GLP-1
CCK

24
Q

what is GLP-1?
role on:

  • satiety [1]
  • insulin & glucagon levels[1]
  • gastric emptying [1]
A

Glucagon like peptide -1

  • inhibits gastric emptying = produces feeling of fullness
  • stimulates: insulin secretion & decreases glucagon (lowers blood glucose)
  • produces rapid satiety
25
Q

CCK, GLP-1, insulin & other peptides stimulate which neurones in the arcuate nucleus? [2]

what effect does this have on satiety? [1]

A

CCK, GLP-1 & other peptides stimulate which neurones in the arcuate nucleus? [2]
POMC
CART

what effect does this have on satiety? [1]
stimulates satiety

26
Q
A
27
Q

what is pancreatic peptide YY hormone’s role?

effect on satiety? how?

A

what is pancreatic peptide YY hormone’s role:

effect on satiety?
increases ileal absorbtion and slows gastric emptying

28
Q

which of the following is produced by adipose tissue?

insulin
ghrelin
leptin
GLP-1
CCK

A

which of the following is produced by adipose tissue?

​insulin
ghrelin
leptin
GLP-1
CCK

29
Q

what does circulating leptin reflect in the body? [2]

A

what does circulating leptin reflect in the body? [2]

  • *total amount of adipose tissue;**
  • *therefore gives brain a reading of total energy storage**
30
Q

which of the following is does not rise rapidly after a meal?

​insulin
ghrelin
leptin
GLP-1
CCK

A

which of the following is does not rise rapidly after a meal?

​insulin
ghrelin
leptin: not related to food intake !!
GLP-1
CCK

31
Q

damage to arcuate nucleus & periventricular nuclei would cause what pathology? [1]

A

damage to arcuate nucleus & periventricular nuclei would cause what pathology? [1]
overeating and obesity (due to loss of ability to detect hormones releesed from gut

32
Q

what are reward pathways of the brain ? & where ?

A

actions of the orofacial muscles during drinking or feeding activate dopamine neurons in the ventral tegmental area of the brainstem: activate **nucleus accumbens (frontal lobe)

e.g.-**
drinking water = enjoy if thirsty or not (important for suckling)
- feeding = pleasurable

33
Q

what has happened to reward pathway for individuals with anorexia?

A

reward pathway has come uncouple from the system fod food intake