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
What's the effect of AgRP binding to the MC4 receptor?
- 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
Which peptides bind to the MC4 receptor at high & low levels of leptin?
- High leptin = alpha MSH released & binds to MC4 -> inhibits feeding - Low leptin = AgRP released & binds to MC4 -> stimulates feeding
27
Define satiety
- Satiety is the feeling of fullness & the suppression of food consumption after a meal for a long period
28
What are the three phases of feeding/digestion?
1. CEPHALIC PHASE 2. GASTRIC PHASE 3. INTESTINAL PHASE
29
What happens in the cephalic phase?
- 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
What happens in the gastric phase?
- The phase during food consumption - Release of mucin & digestive secretions in response to chewing or swallowing - Gastric distension of stomach
31
What happens in the intestinal phase?
- Food is transported from distended stomach to intestines for intestinal phase - Cholecystokinin released in response to fatty foods by the intestine
32
What are three satiety signals in the short term regulation of feeding?
1. GASTRIC DISTENSION 2. CCK (Cholecystokinin) 3. INSULIN
33
How does gastric distension act as a short term satiety signal?
- Gastric distension signals to the nucleus solitarius tract (NTS) via the vagus nerve to inhibit feeding
34
How does cholecystokinin act as a short term satiety signal?
- CCK acts on vagus nerve to inhibit feeding
35
How does insulin act as a short term satiety signal?
- 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
How is dopamine involved in feeding behaviour?
- 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
What is positive & negative reinforcement?
- Positive reinforcement - repeating a behaviour due to pleasant or rewarding effect - Negative reinforcement - repeating a behaviour to avoid an unpleasant experience
38
What's the link between dopamine & positive reinforcement?
- 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
What's the link between dopamine & negative reinforcement?
- Suppression of the mesolimbic pathway is associated with negative reinforcement
40
How is positive & negative reinforcement involved in addiction?
- 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
What happens to D2 receptors in individuals suffering from obesity or addiction?
- 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
What happens to D2 receptors in individuals with depression?
- There's a downregulation of D2 receptors in individuals with depression - Leads to decreased interest in activities that would normally be rewarding
43
How is serotonin involved in feeding behaviour?
- 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