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PSYCH310 > WEEK 9- HUNGER AND SATIETY III: CENTRAL FACTORS- SEROTONIN AND MONOAMINES > Flashcards

WEEK 9- HUNGER AND SATIETY III: CENTRAL FACTORS- SEROTONIN AND MONOAMINES Flashcards

1
Q

What is the main site of action for hunger and satiety?

A

hypothalamus

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2
Q

what parts of the hypothalamus are involved in hunger and satiety?

A

DMH, VMH, ARC and LHA

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3
Q

what does the hypothalamus integrate?

A

multiple signals from areas in the body such as the gut and liver and works out the best course of action

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4
Q

what process is serotonin mainly associated with?

A

satiety

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5
Q

what does orexigenic mean?

A

stimulates food intake

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6
Q

what does anorexigenic mean?

A

inhibit food intake

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7
Q

what is hyperphagia

A

excess food intake

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8
Q

what is hypophagia

A

reduced food intake

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9
Q

what neuropeptides are associated with hyperphagia

A

NPY, Orexin A, MCH, AGRP and opioids

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10
Q

what neuropeptides and neurotransmitters are associated with hypophagia?

A

a-MSH, serotonin, CART, GLP-1, CRF

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11
Q

What is serotonin?

A

a monoamine neurotransmitter found in the brain

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12
Q

what is the main site of expression for serotonin?

A

raphe nuclei - located on the midline of the brainstem. 5-HT produced in the raphe nuclei is transported to and released at numerous brain sites- acts via serotonin receptors of which various subtypes exist

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13
Q

how many different types of serotonin receptors are found throughout the brain?

A

18

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14
Q

what amino acid does serotonin come from?

A

tryptophan

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15
Q

where do we get tryptophan from?

A

diet

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16
Q

what happens once we consume tryptophan?

A

enters the brain then hydrolysed into 5-HTP then serotonin

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17
Q

what is serotonin further metabolised into?

A

5-HIAA

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18
Q

what is an example of a drug that mimics the effects of 5-ht or increase 5-ht availability?

A

fluxetine (prozac)- a selective serotonin reuptake inhibitor

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19
Q

what does antagonists of serotonin do?

A

block the effects of 5-ht eg metergoline

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20
Q

what do serotonin agonists do?

A

increase the activity of serotonin in the brain

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21
Q

what do SSRI’S do

A

block the reuptake of serotonin from the receptors

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22
Q

where are neurotransmitters released

A

presynaptic terminal

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23
Q

what happens to the neurotransmitter once released from the presynaptic terminal

A

travels across the synapse

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24
Q

what does serotonin do (with regards to appetite)

A

5-ht reduces food intake and weight gain in both rodents and humans. it also enhanced energy expenditure

25
Q

where does serotonin have its effects?

A

the hypothalamus is a key site. sites outside the hypothalamus fail to exhibit any repsonse to 5-ht injection. hindbrain nuclei may play a role. however injections of fenfluramine (5-ht agonist) continue to reduce food intake even if the paraventricular nucleus within the hypothalamus has been destroyed ie effects of serotonin are not entirely dependent on hypothalamic structures

26
Q

what study shows serotonins impact on eating patterns?

A

blundell 1986- design: monitor changes in the behavioural structure of feeding in rats in conjunction with various pharmacological treatments. findings: 5-ht induces a significant decrease in the size and duration of individual meals. 5-ht is associated with a reduced rate of eating. conclusion: results indicate that 5-ht enhances satiation and prolongs satiety (inhibition of further eating) - this was one of the first studies that got into the nitty gritty of what serotonin does and how it affects appetite. also found they could go longer without a meal

27
Q

what study by lawton et al 1995 also showed the effects of serotonin on eating patterns

A

female participants with obesity felt less hungry when fluoxetine than placebo. fluoextine reduced energy intake relative to placebo. fluoxetine treatment produced significant weight loss over two weeks of treatment

28
Q

what is serotonin’s impact on food choice?

A

traditonally 5-ht has been linked to the macronutrient carbphydrate (CHO). 5-ht specifically terminates CHO rich meals, reduces the rate of CHO eating and enhances satiating effects of CHO. proposed to influence the ratio of CHO to protein by reducing the proportion of CHO in the diet. reduction in fat intake only observed at higher doses

29
Q

what does tryptophan compete with?

A

other amino acids- to cross the blood brain barrier

30
Q

what does the consumption of carbohydrates increase?

A

plasma ratio of tryptophan to other amino acids. this promotes trypophans entry into the brain where it is converted to 5-ht

31
Q

what mechanism does 5-ht acts as

A

negative feedback mechanism to reduce subsequent carbohydrate consumption

32
Q

what does insulin have little or no effect on?

A

plasma tryptophan levels

33
Q

what does insulin lower?

A

plasma levels of the ‘large neutral amino acids’ (LNAA) which compete with tryptophan for passage across the blood brain barrier

34
Q

what is thought to underlie carbohydrate craving?

A

disturbances in the 5-ht negative feedback mechanism- seen in seasonal affective disorder and pre-menstrual syndrome

35
Q

what underlies the associated binge eating sometimes seen in female dieters- wurtman and wurtman 1995

A

decreases in brain tryptophan and 5-ht caused by low carbohydrate weight-loss diets - low levels of serotonin= binge eating due to less satiety

36
Q

what receptor subtype has been implicated extensively in the regulation of ingestive behaviour

A

the 5-ht (2c) receptor subtype

37
Q

what do mice lacking the 5-HT (2c) receptor develop?

A

obesity

38
Q

what does the 5-HT(2C) agonist mcPP reduce?

A

weight gain in rats

39
Q

what is the 5-HT(6) receptor identified as?

A

novel ‘feeding receptor’

40
Q

what did Thomas et al 2014 examine the effects of?

A

examined the effects of the 5-HT2C receptor agonist mcPP on appetite and mood in healthy human volunteers

41
Q

what was the finding of the Thomas et al 2014 study on mcPP?

A

mcPP reduced appetite and in women, enhanced measures of within- meal satiation relative to placebo. but no significant effect on food intake. memory for emotional material was also enhanced (remember increased appetite doesn’t always mean increased food intake)

42
Q

what is the current rationale on serotonin and leptin?

A

functioning in separate circuits- serotonin involved in episodic satiety and leptin involved in tonic satiety (long term)

43
Q

what is the evidence for parallel circuits for serotonin and leptin?

A

5-ht drugs activate ARC POMC neurones via 5-HT(2C) receptors. 5-ht inhibits the activity of ARC NPY neurones

44
Q

which episodic peripheral factors signal satiety?

A

CCK, PYY, BOMBESIN

45
Q

what study shows the effects of serotonin on CCK?

A

gringnaschi et al 1993- the effect of d-funfluramine (5-HT agonist) on food intake in rats were partially blocked by the CCKa receptor antagonist, devazepine. the effects of CCK on meal size were completely blocked by the 5-HT receptor antagonist, metergoline. conclusion: a reciprocal interaction exists between 5-HT and CCK. 5-HT and CCK act in a network for episodic satiety signalling. the participants were given either drugs that targeted the 5-HT system or the CCK system. when rats are adiministered with CCK this reduced food itnake but when also administered with 5-HT agonist this effect was blocked

46
Q

what study showed that fat is a potent stimulus for CCK release?

A

blundell et al 1995- diet selection studies in rodents and humans indicate prominent reduction in fat. 5-ht activation in humans can lead to selective avoidance of fat in the diet. fat in the intestine is a potent stimulus for CCK release- may involve CCK in a pre-abosrptive mechanism, we know detection of fat within the intestine causes CCK to be released- which is a satiety signal- tells brain food has been ingested

47
Q

what is the suggestion about the serotonin system and eating disorders?

A

deficiencies or malfunctioning of the 5-ht system may contribute or cause eating disorders

48
Q

what suggests anorexia is not caused by modern cultural factors?

A

clear descriptions of AN date from the middle of the 19th century- this suggests other factors may be contributing

49
Q

individual with obesity have reduced levels of what?

A

5-HT

50
Q

what has reduction of 5-ht been negatively correlated with?

A

BMI

51
Q

what does dieting reduce?

A

plasma tryptophan (5-HT precursor) and thus CNS levels of 5-HT in healthy women

52
Q

low levels of what are observed in patients with frequent binge episodes?

A

low CNS 5-HT levels - been shown if you go on a diet there is a reduction in brain tryptophan

53
Q

what study showed the effect of bulimia on serotonin levels

A

Jimerson et al 2012- 12 bulimic women, who binge at least 3 times a week were matched with 17 healthy controls, CSF was collected by a lumbar puncture, CSF was analysed for the concentration of the 5-HT metabolite 5-HIAA. results: compared to control the BN group had lower CSF 5-HIAA, within the BN group the binge frequency negatively correlated with CSF 5-HIAA levels. low 5-HIAA indicates low CNS 5-HT

54
Q

what does removing tryptophan from the diet of patients with BN lead to?

A

reduced mood such as depression, sadness and mood liability, increasing body concern, increased feeling of loss of control over eating and desire to binge

55
Q

what study shows the effects of removing tryptophan from the diets of BN patients?

A

smith et al 1999- 10 patients with BN and 12 matched healthy females. given 86g amino acid mix lacking tryptophan, asked to self- rate i) mood ii) eating cognitions for 7 hours post administration. results: BN individuals had greater lowering of mood, increased body image concern and subjective loss of control of eating compared to the healthy controls. diminished 5-HT activity may trigger cognitive and mood disturbances in BN. chronic tryptophan depletion may also occur with dieting and may lead to development of disordered eating

56
Q

what is further evidence for disturbed 5-HT

A

prolactin response test- used 5-HT drugs to challenge the endogenous 5-HT system. the rise in plasma prolactin level following administration of 5-HT drug is taken as an index of 5-HT responsivity. patients ith bulimia nervosa have weak prolactin repsonses. they possess decreased 5-HT functioning. this is associated with binge eating frequency. when 5-ht is released there is also increase in prolactin- can monitor this response to see how well 5-ht drug has worked. those with bulimia have a slow increase in prlacti when administered with the drug

57
Q

what study shows the effects of eating disorders on prolactin response

A

Jimerson et al 1997- 15 patients with BN who had binged 3 times per week for 6 months compared to healthy controls. given 60mg fenfluramine (5-HT agonist) or placebo. blood taken every hour over next 5 hours and analysed prolactin levels. results: in the patients, serum prolactin level repsonse was blunted compared to control (drug vs placebo). within the patient group, frequency of binge eating within the previous month correlated negatively with prolactin response. impaired 5-ht response is observed in patients with BN and this is significantly associated with binge eating symptomology

58
Q

what is the most compelling evidence for 5-HT disturbance in eating disorders?

A

kaye et al 1998- the positive response to anti-depressant medication. the 5-ht reuptake inhibitor fluoxetine reduces binge frequency, improves mood disturbances and preoccupation with shape and weight

59
Q

what is the evidence for 5-ht receptor sensitivity in eating disorders?

A

receptor sensitivity can be determined by measuring prolactin response to specific receptor agonists. dieting reduces plasma tryptophan and thus levels of 5-HT in healthy women (wolfe et al 1997). BUT an increased prolactin response has been found in normal weight women but not men following dieting (goodwin et al 1987). this may be a result of 5-HT2c receptor super-sensitivity ie upregulating the repsonsiveness of of central 5-HT pathways

PSYCH310 (9 decks)

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