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brain and behaviour > neural control of motivational behaviour > Flashcards

neural control of motivational behaviour Flashcards

1
Q

what are circumventricular organs?

A

structures where the BBB is leaky at some points bc of fenestrated capillaries

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2
Q

where are circumventricular organs found?

A

surround the ventricular system

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3
Q

name some circumventricular organs

A 
area postrema
posterior pituitary
median eminence
subfornical organ
subcommissural organ 
pineal gland
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4
Q

what can cause blood osmolarity to increase?

A

o if total body water is low bc of sweating/lack of drinking t

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5
Q

what senses blood osmolarity?

A

sensed by osmoreceptor cells in the subfornical organ – a circumventricular organ

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6
Q

explain the pathway of detecting high blood osmolarity and how this is kept under control?

A
  • subfornical organ detects
    high blood osmolarity
  • activates cells in medial preoptic nucleus of hypothalamus
  • nucleus projects into limbic system –> regulates thirst
  • cells of the paraventricular and supraoptic nucleus are also activated
  • their axons project to the posterior pituitary –> release ADH –> reduce urine -> reduce water loss in urine -> prevents blood osmolarity rising even further
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7
Q

which nucleus makes us feel thirst?

A

medial preoptic nucleus

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8
Q

where is the paraventricular nucleus found?

A

around the 3rd ventricle

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9
Q

where is the supraoptic nucleus found?

A

above the optic chiasm

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10
Q

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

A
  • aquaporins: more move into the collecting duct epithelial membranes. water moves into renal medulla - less urine, higher conc
  • increases collecting duct permeability to urea
  • stimulates Na+ reabsorption in the ascending loop of Henle through the Na+ K+ 2CL- cotransporter. Increases osmolarity of medullary extracellular fluid -> more water reabsorbed from collecting ducts
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11
Q

what does the body do when water is lost by sweat during heat stress?

A

we drink more water to compensate

Body also increases aldosterone secretion and decreases atrial natriuretic peptide secretion -> decreases sodium loss in urine -> compensates for sodium loss in the sweat and prevents hyponatraemia

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12
Q

which 2 factors initiate feeding behaviour?

A

o External cue – immediate availability of food

o Internal cue – sense of hunger from inside your body

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13
Q

what is the major store of energy in mammals?

A

adipose tissue

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14
Q

what is weight maintained by?

A

o Adipostatic model – factors released by fat target the hypothalamus to control feeding and maintain weight
o Intestinal absorption - altering intestinal transit time –> altering absorption of caloric material in the intestine

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15
Q

describe the early evidence for the role of the hypothalamus in appetite?

A

o Patients with pituitary tumours pressing up on the hypothalamus demonstrated voracious appetite, morbid obesity and hypogonadism – known as adiposogenital syndrome

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16
Q

what do lesions in the lateral hypothalamus cause?

A

anorexia

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17
Q

what do lesions in the medial hypothalamus cause?

A

obesity

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18
Q

what does the ventromedial satiety centre do?

A

inhibited feeding when stimulated

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19
Q

what stimuli does the hypothalamus respond to to regulate food intake?

A

o Internal stimuli – contraction of the stomach, the levels of various blood chemicals e.g. glucose, insulin, ghrelin, cholecystokinin and leptin
o External stimuli – sight and smell of food

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20
Q

what does whether we eat food or not depend on?

A

the balance between external stimuli (how attractive the food is) and internal stimuli (how hungry we feel)

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21
Q

what does the arcuate nucleus detect?

A

internal cues e.g. levels of blood hormones

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22
Q

what do arcuate lesions do?

A

destroy the animal’s ability to detect internal signals

o If presented with palatable food, it will eat until it can physically eat no more
o If presented with unpalatable food, it will starve to death as it has no ability to detect internal hunger signals

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23
Q

what are the main cell types in the arcuate and periventricular nuclei?

A

o ‘Agouti-related peptide*’ (AGRP) & ‘Neuropeptide Y’ neurones (NPY) neurones
o ‘Cocaine & amphetamine related transcript’ neurones (CART) & ‘Pro-opiomelanocortin (POMC)’ neurones

24
Q

what is ghrelin?

A

hunger hormone

protein hormone produced by special ghrelinergic cells

25
Q

where are ghrelinergic cells found?

A

found mainly in the fundus, but also in other parts of gut e.g. duodenum and ileum (to a lesser extent) and epsilon cells of the pancreas

26
Q

what detects stomach contractions and where does this signal?

A

vagus nerve

signals to the hypothalamus and the brainstem

27
Q

when is ghrelin released?

A

when the stomach contracts

when blood glucose is low

28
Q

what does ghrelin do?

A

• Generates hunger by action on (NPY) and (AGRP) cells in arcuate nucleus
- stimulates dopamine pathway in brain –> responsible for hedonic aspect of eating

29
Q

what type of receptors are ghrelin receptors?

A

G protein-coupled receptors

30
Q

how does ghrelin generate a sense of hunger?

A

stimulate action on NPY and AGRP cells in the arcuate nucleus

these neurons stimulate neurons in the limbic system that mediate hunger sensation and inhibit ‘satiety’ (POMC & CART) neurons

31
Q

what is cholecystokinin?

A

a peptide synthesised by cells in the mucosal epithelium of the small intestine and secreted into the duodenum when food moves from stomach –> duodenum

32
Q

what does CCK do?

A
  • Causes release of digestive enzyme from pancreas and bile from gallbladder
  • Released into the blood and travels to the hypothalamus
  • CCK acts on cells in arcuate nucleus to produce satiety –> a satiety signal
33
Q

what is glucagon like peptide 1?

A

• Hormone released as a result of food in the gut

34
Q

what does GLP-1 do?

A
  • Produces rapid satiety by an action on the arcuate cells
  • Inhibits gastric emptying –> produces a feeling of fullness
  • Stimulates insulin secretion and decreases glucagon –> lowers blood glucose
35
Q

what do CCK, GLP-1 and other peptides do?

A

stimulate feeding stimulate neurones in the arcuate nucleus that contain POMC & CART

These neurons stimulate sense of satiety + stop feeding behavior

36
Q

what is PPY?

A

• Pancreatic peptide YY – large peptide hormone synthesised within gastrointestinal tract in L cells

37
Q

what are L cells?

A

specialised enteroendocrine cells

38
Q

what does PPY do?

A

increases ileal absorption, slows gastric emptying and delays gallbladder and pancreatic secretion

39
Q

what is leptin?

A

protein hormone produced by adipose tissue

40
Q

what does the amount of circulating leptin reflect?

A

reflects total amount of adipose tissue in the body and therefore gives brain a reading of total energy storage
o Tells hypothalamus whether the body is above its set point weight or below it

41
Q

what does deletion of leptin receptors in the hypothalamus cause?

A

induces chronic obesity

42
Q

why is leptin a long term regulator of appetite?

A

• Leptin levels don’t rise rapidly after a meal –> cannot be a fast acting ‘satiety signal’ to stop eating
modulates response to fast acting satiety signals

43
Q

how can leptin affect fertility?

A

Woman ceases to menstruate and ovulate if circulating leptin decreases below a certain level bc it prevents gonadotrophic hormones from being released.

44
Q

what does arcuate+ adjacent hypothalamic nuclei damage cause?

A

reduces ability to sense internal cues

feeding behaviour therefore controlled by external cues alone

45
Q

what does a ventromedial lesion cause?

A

will cause a person to overeat if given palatable food but starve if given unpalatable food –> people become picky with their diet

46
Q

what do lesions in the lateral hypothalamus cause?

A

anorexia

47
Q

why are lesions in the lateral hypothalamus difficult to interpret?

A

these lesions may interrupt several neuronal pathways e.g. dopamine pathways which destroy pleasure of eating

48
Q

what are reward pathways in the brain?

A

brain systems that are active when you feel happy

49
Q

why are reward pathways important in babies?

A

act of suckling activates this pathway

if it didn’t activate this pathwy then the baby would not feed and die

50
Q

how is the act of chewing rewarding?

A

o Actions of the orofacial muscles during drinking or feeding activate dopamine neurons in the ventral tegmental area of the brainstem  project to and activate neurons in the nucleus accumbens (found deep in the frontal lobe)
o Activation of the accumbens neurons is the neuronal correlate of feelings of pleasure/reward

51
Q

what is anorexia nervosa?

A

• An eating disorder characterised by low weight, fear of gaining weight and a strong desire to be thin, resulting in voluntary food restriction

52
Q

what are complications of anorexia?

A

osteoporosis, infertility, and heart damage. Women will stop having menstrual periods.

53
Q

how is the severity of anorexia classified?

A 
based on BMI
Mild disease is a BMI of 17-18
moderate a BMI of 16-17, 
severe a BMI of 15-16
extreme a BMI less than 15.
54
Q

how is anorexia partly a psychological perceptual problem?

A

view themselves as overweight when they aren’t, usually deny having a problem with low weight, weigh themselves frequently, only eat small amounts etc

55
Q

what pathway is affected in anorexics?

A

Reduced pleasure from orofacial activity – suggests that the reward pathway has been uncoupled from food intake system  eating and drinking is no longer rewarding for them

brain and behaviour (24 decks)

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