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Flashcards in neural control of motivational behaviour Deck (55):
1

what are circumventricular organs?

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

2

where are circumventricular organs found?

surround the ventricular system

3

name some circumventricular organs

area postrema
posterior pituitary
median eminence
subfornical organ
subcommissural organ
pineal gland

4

what can cause blood osmolarity to increase?

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

5

what senses blood osmolarity?

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

6

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

- 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

7

which nucleus makes us feel thirst?

medial preoptic nucleus

8

where is the paraventricular nucleus found?

around the 3rd ventricle

9

where is the supraoptic nucleus found?

above the optic chiasm

10

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

- 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

11

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

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

12

which 2 factors initiate feeding behaviour?

o External cue – immediate availability of food
o Internal cue – sense of hunger from inside your body

13

what is the major store of energy in mammals?

adipose tissue

14

what is weight maintained by?

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

15

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

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

16

what do lesions in the lateral hypothalamus cause?

anorexia

17

what do lesions in the medial hypothalamus cause?

obesity

18

what does the ventromedial satiety centre do?

inhibited feeding when stimulated

19

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

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

20

what does whether we eat food or not depend on?

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

21

what does the arcuate nucleus detect?

internal cues e.g. levels of blood hormones

22

what do arcuate lesions do?

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

23

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

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

24

what is ghrelin?

hunger hormone
protein hormone produced by special ghrelinergic cells

25

where are ghrelinergic cells found?

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

what detects stomach contractions and where does this signal?

vagus nerve
signals to the hypothalamus and the brainstem

27

when is ghrelin released?

when the stomach contracts
when blood glucose is low

28

what does ghrelin do?

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

29

what type of receptors are ghrelin receptors?

G protein-coupled receptors

30

how does ghrelin generate a sense of hunger?

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

what is cholecystokinin?

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

what does CCK do?

• 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

what is glucagon like peptide 1?

• Hormone released as a result of food in the gut

34

what does GLP-1 do?

• 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

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

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

These neurons stimulate sense of satiety + stop feeding behavior

36

what is PPY?

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

37

what are L cells?

specialised enteroendocrine cells

38

what does PPY do?

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

39

what is leptin?

protein hormone produced by adipose tissue

40

what does the amount of circulating leptin reflect?

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

what does deletion of leptin receptors in the hypothalamus cause?

induces chronic obesity

42

why is leptin a long term regulator of appetite?

• 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

how can leptin affect fertility?

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

44

what does arcuate+ adjacent hypothalamic nuclei damage cause?

reduces ability to sense internal cues

feeding behaviour therefore controlled by external cues alone

45

what does a ventromedial lesion cause?

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

46

what do lesions in the lateral hypothalamus cause?

anorexia

47

why are lesions in the lateral hypothalamus difficult to interpret?

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

48

what are reward pathways in the brain?

brain systems that are active when you feel happy

49

why are reward pathways important in babies?

act of suckling activates this pathway

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

50

how is the act of chewing rewarding?

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

what is anorexia nervosa?

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

52

what are complications of anorexia?

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

53

how is the severity of anorexia classified?

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

how is anorexia partly a psychological perceptual problem?

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

what pathway is affected in anorexics?

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