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PHYS - NEURO > 13. MOTIVATION > Flashcards

13. MOTIVATION Flashcards

1
Q

Define motivation

A
  • Motivation refers to the driving force of physical need to do something
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2
Q

When does anabolism & catabolism occur in regards to feeding?

A
  • Metabolism is a combination of both anabolism & catabolism
  • Anabolism occurs during the prandial state (eating), where excess glucose, fatty acids are stored
  • Catabolism occurs during the post-prandial state (after eating) where the trigylceride, glycogen stores etc. are broken down
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3
Q

What is the parabiosis experiment of mice?

A
  • Parabiosis = fusion
  • An obese mice with a defect in the ob gene (ob/ob), so it was unable to produce leptin
  • This obese mice was fused to a normal mice, so that their circulation was shared
  • Researchers found the obese mouse lost weight & it’s weight matched that of the control mouse
  • The leptin from the normal mouse entered the circulation of the ob/ob mouse & acted on leptin receptors to regulate feeding
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4
Q

What is a satiety signal involved in the long term hormonal regulation of feeding?

A
  • Leptin is involved in the long-term hormonal regulation of feeding
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5
Q

What is leptin?

A
  • Leptin is satiety signal
  • It is released by adipose tissue, when fat stores are replenished to regulate feeding
  • High levels of leptin -> full, inhibits feeding
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6
Q

Where are leptin receptors?

A
  • Leptin is released from adipose tissue & acts on the leptin receptor
  • The leptin receptor is located in the arcuate nucleus
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7
Q

What does a lesion of the lateral hypothalamus cause?

A
  • LATERAL HYPOTHALMUS = lose weight (anorexia), decreased appetite
  • Results in lateral hypothalamic syndrome
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8
Q

What does a lesion of the ventromedial hypothalamus cause?

A
  • VENTROMEDIAL HYPOTHALAMUS = obesity/weight gain, increased appetite
  • Results in ventromedial hypothalamic syndrome
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9
Q

What are anorectic peptides?

A
  • Anorectic peptides SUPPRESS appetite, inhibit feeding

- Endogenous neuropeptides such as alpha-MSH or CART

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10
Q

What are orexigenic peptides?

A
  • OREXIGENIC peptides INCREASE appetite, stimulate feeding

- Endogenous peptides such as AgRP, NPY, orexin, MCH, Ghrelin

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11
Q

What two anorectic peptides are released in response to high leptin?

A
  1. Alpha-MSH (Alpha - melanocyte stimulating hormone)

2. CART (Cocaine-amphetamine regulated transcript)

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12
Q

Where are alpha MSH & CART released from?

A
  • Alpha- MSH & CART are released from alpha-MSH & CART neurones in the arcuate nucleus
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13
Q

Where do alpha MSH & CART neurones project to & how do they inhibit feeding?

A
  1. LATERAL HYPTHALAMIC AREA - inhibit feeding
  2. PARAVENTRICULAR NUCLEUS - stimulates neurones which release ACTH & TSH from anterior pituitary to increase metabollic rate
  3. BRAIN STEM - stimulate sympathetic activity
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14
Q

What is the response to high leptin called?

A
  • Anorexic response

- Aims to inhibit feeding

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15
Q

What is the response to low leptin called?

A
  • Orexigenic response

- Aims to increase feeding

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16
Q

What are two orexigenic peptides released in response to low leptin?

A
  1. AgRP (agouti-related peptide)
  2. NPY (Neuropeptide Y)
    - Stimulate appetite
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17
Q

Where are AgRP & NPY released from?

A
  • AgRP & NPY are released by arcuate AgRP & NPY neurones in the arcuate nucleus
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18
Q

How are leptin levels detected?

A
  • Leptin receptors are in the arcuate nucleus
  • High or low levels of leptin will be detected by the arcuate nucleus
  • Either anorectic or orexigenic peptides will be released by arcuate neurones (AgRP, NPY, CART or alpha MSH)
19
Q

Where do the AgRP & NPY neurones project to & how do they stimulate feeding?

A
  1. LATERAL HYPOTHALAMIC AREA - stimulate feeding
  2. PARAVENTRICULAR AREA - inhibits neurones which cause release of ACTH & TSH by anterior pituitary to decrease basal metabolic rate
  3. BRAIN STEM - inhibit sympathetic activity & stimulate parasympathetic activity
20
Q

How do projection of AgRP & NPY to the lateral hypothalamus stimulate feeding?

A
  • The arcuate AgRP & NPY neurones project to the lateral hypothalamus to stimulate feeding
  • The lateral hypothalamus produces orexigenic peptides to stimulate appetite:
    1. OREXIN
    2. MELANIN CONCENTRATING HORMONE
21
Q

Where are orexin & MCH released from & what do they do?

A
  • Orexin & MCH are released from the lateral hypothalamus
  • They are orexigenic peptides
  • Orexin = promotes meal initiation
  • MCH = prolongs consumption of food
22
Q

What two competitive peptides bind to MC4 receptor?

A
  1. alpha MSH
  2. AgRP
    - Both bind to MC4 and have opposite effects
23
Q

Where are MC4 receptors located?

A
  • Hypothalamic neurones
24
Q

What’s the effect of alpha MSH binding to the MC4 receptor?

A
  • alpha-MSH is an agonist for MC4 receptor

- Binding of alpha-MSH inhibits feeding

25
Q

What’s the effect of AgRP binding to the MC4 receptor?

A
  • AgRP is a competitive antagonist for the MC4 receptor

- Binding to teh MC4 receptor counteracts the effects of alpha-MSH to stimulate appetite rather than inhibit it

26
Q

Which peptides bind to the MC4 receptor at high & low levels of leptin?

A
  • High leptin = alpha MSH released & binds to MC4 -> inhibits feeding
  • Low leptin = AgRP released & binds to MC4 -> stimulates feeding
27
Q

Define satiety

A
  • Satiety is the feeling of fullness & the suppression of food consumption after a meal for a long period
28
Q

What are the three phases of feeding/digestion?

A
  1. CEPHALIC PHASE
  2. GASTRIC PHASE
  3. INTESTINAL PHASE
29
Q

What happens in the cephalic phase?

A
  • Cephalic phase is the phase in anticipation to a meal
  • Increased saliva secretion
  • Ghrelin released from empty stomach
  • Activation of AgRP & NPY neurones in arcuate nucleus
  • Parasympathetic nervous system & enteric nervous system activation
30
Q

What happens in the gastric phase?

A
  • The phase during food consumption
  • Release of mucin & digestive secretions in response to chewing or swallowing
  • Gastric distension of stomach
31
Q

What happens in the intestinal phase?

A
  • Food is transported from distended stomach to intestines for intestinal phase
  • Cholecystokinin released in response to fatty foods by the intestine
32
Q

What are three satiety signals in the short term regulation of feeding?

A
  1. GASTRIC DISTENSION
  2. CCK (Cholecystokinin)
  3. INSULIN
33
Q

How does gastric distension act as a short term satiety signal?

A
  • Gastric distension signals to the nucleus solitarius tract (NTS) via the vagus nerve to inhibit feeding
34
Q

How does cholecystokinin act as a short term satiety signal?

A
  • CCK acts on vagus nerve to inhibit feeding
35
Q

How does insulin act as a short term satiety signal?

A
  • Insulin is released by the beta cells of the pancreas
  • It’s released in response to excess circulating glucose
  • It acts on the arcuate nucleus to induce satiety
36
Q

How is dopamine involved in feeding behaviour?

A
  • Dopaminergic neurones are involved in releasing dopamine, to cause the wanting fro food
  • Dopamine involved in motivation but not liking (not involved in hedonic aspect)
  • Mesolimbic pathway - dopaminergic neurones project from the VTA to nucleus accumbens
37
Q

What is positive & negative reinforcement?

A
  • Positive reinforcement - repeating a behaviour due to pleasant or rewarding effect
  • Negative reinforcement - repeating a behaviour to avoid an unpleasant experience
38
Q

What’s the link between dopamine & positive reinforcement?

A
  • Release of dopamine in the nucleus accumbens is thought to drive positive reinforcement behaviour
  • However, dopamine is only involved in the motivational aspect not the hedonic aspect (not involved in liking)
39
Q

What’s the link between dopamine & negative reinforcement?

A
  • Suppression of the mesolimbic pathway is associated with negative reinforcement
40
Q

How is positive & negative reinforcement involved in addiction?

A
  • Release of dopamine in nucleus accumbens drives the addiction = POSITIVE REINFORCEMENT
  • However, dependence on the source of addiction can lead to withdrawal effects when stopped.
  • Individuals continue to use substance or source of addiction to avoid the unpleasant effects of withdrwal = NEGATIVE REINFORCEMENT
  • In addicted individuals, the drugs are thought to act on amygdala not GABAergic neurones
41
Q

What happens to D2 receptors in individuals suffering from obesity or addiction?

A
  • There’s a downregulation of D2 receptor expression
  • Decrease in D2 receptors is correlated with increased craving & a vulnerability to relapse
  • Rewarding effects are reduced, so individuals need to increase the dosage
42
Q

What happens to D2 receptors in individuals with depression?

A
  • There’s a downregulation of D2 receptors in individuals with depression
  • Leads to decreased interest in activities that would normally be rewarding
43
Q

How is serotonin involved in feeding behaviour?

A
  • Serotonin is released in the hypothalamus in anticipation to a meal & spikes during a meal
  • Low serotonin levels are associated with anorexia nervosa, bullimia & depression. Co-morbidity with these disorders

PHYS - NEURO (18 decks)

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