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Neuro > Motivation > Flashcards

Motivation Flashcards

1
Q

What is motivation?

A

A driving force e.g. physical need, wanting, liking etc

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2
Q

Function of the hypothalamus

A

Key regulator for maintaining homeostasis by regulating three interrelated functions:

  • Endocrine secretion
  • Autonomic nervous system
  • Emotions and drive/behaviour e.g. motivated behaviour e.g. drinking, eating
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3
Q

Describe the loading and emptying the body’s energy reserves

A
  • Following consumption of a meal, there is absorption of nutrients into the blood circulation.
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4
Q

What happens to excess glucose from a meal?

A
  • Stored as glycogen in the liver and muscles

- Also be storage of triglycerides in adipose tissues

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5
Q

What happens during periods of starvation?

A

Breakdown of glycogen to glucose and breakdown of adipose fat tissue into triglycerides which will then further break down into glucose, fatty acids and ketone bodies.

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6
Q

What metabolisms are regulated by the hypothalamus?

A

Both the anabolism and catabolism reactions are tightly regulated.

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7
Q

How is a normal weight maintained?

A

If there is a balance between intake and energy expenditure this will result in a normal weight.

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8
Q

What happens if there is a greater intake compared to expenditure?

A

Results in obesity

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9
Q

What happens if there is a lower intake compared to energy expenditure?

A

Results in starvation

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10
Q

Where does the transduction of physiological stimuli in the blood occur?

A

In a specialised region of the hypothalamus

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11
Q

What initiates humoral and visceromotor responses?

A

Initiated by activation periventricular and medial hypothalamus

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12
Q

What does behavioural action depend on?

A

Depends on lateral hypothalamus

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13
Q

Why was it assumed that there was a protein involved in feeding?

A

In the 50s, they assumed there must be a molecule/protein released in the blood circulation following feeding that would suppress appetite.

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14
Q

What is parabiosis?

A

The sharing of blood circulation between animals

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15
Q

Explain the mice parabiosis experiement

A
  • A genetically obese mouse with the ob/ob gene had fat cells that did not produce leptin inhibiting food intake.
  • It was connected to a normal mouse like siamese twins which produces leptin leading to a reduction of obesity in the ob/ob mouse.
  • After 3-4 weeks, the obese mouse started to have a reduced food intake and lose weight.
  • This showed that following parabiosis, the normal mouse was producing the protein leptin which would act on the hypothalamus on the ob/ob mouse meaning it would lose weight as reduced intake of food.
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16
Q

Who discovered the leptin protein?

A

Jeffrey Friedman

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17
Q

Why was leptin not use as an anti-obesity drug?

A

Pharmaceuticals thought that leptin would be the new anti-obesity drug but found that leptin would only cause weight loss if they had abnormal levels of leptin. The majority of obese people had normal leptin levels.

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18
Q

What happens in the body following feeding?

A

Adipose tissue releases leptin into the blood circulation, this eventually acts on a specific region of the hypothalamus which has leptin receptors called the arcuate nucleus. This tells the body to stop eating. This regulates appetitie.

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19
Q

What are the ventromedial and lateral hypothalamus important for?

A

Important for the regulation of:

  • Body weight/food intake
  • Blood volume/osmolarity: drinking
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20
Q

Structure of the frontal section of the hypothalamus

A

Arcuate nucleus is found at the bottom of the third ventricle.
Paraventricular nucleus is adjacent to the left lateral ventricle.
Lateral hypothalamus is found underneath the paraventricular nucleus.

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21
Q

What happens when there is lesions in the ventromedial hypothalamus?

A

When lesions in the VMH, causes excessive eating and obesity. This tells us that the VMH is important for the maintenance of body weight.

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22
Q

What is lateral hypothalamic syndrome?

A

Diminished appetite for food; anorexia normally.

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23
Q

What is the lateral hypothalamus?

A

The hunger centre

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24
Q

What is ventromedial hypothalamic syndrome?

A

Overeating and obestiy

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25
Q

What is the ventromedial hypothalamus?

A

The satiety centre

26
Q

Function of the arcuate nucleus

A

Important for control of feeding

27
Q

Describe the anorexic response

A
  1. There is a rise of elevated leptin levels
  2. Leptin acts on leptin receptors on the arcuate nucleus of the hypothalamus
  3. This will cause the stimulation of arcuate alpha-MSH (melanocyte-stimulating hormone) /CART (cocaine and amphetamine-regulated transcript) neurons which causes the release of neurotransmitter peptides alpha-MSH and CART.
  4. Anorectic peptide will diminish appetite
  5. These neurons will project from the arcuate nucleus to the lateral hypothalamus which will inhibit feeding.
  6. This will also project to the paraventricular nucleus where they stimulate release of ACTH and thyrotropin which increases basal metabolic rate and sympathetic activation.
28
Q

Describe the orexigenic response

A
  1. Adipose tissue is not replenished with FAs, leptin levels are low.
  2. Low leptin means inhibition of alpha-MSH/CART neurons and activation of NPY/AgRP neurons.
  3. NPY/AgRP neurons will project to the lateral hypothalamus and stimulate feeding behaviour.
  4. NPY/AgRP neurons project to the paraventricular nucleus and inhibit the secretion of ACTH and TSH which causes the basal metabolic rate to go down and parasympathetic activation.
29
Q

Orexigenic Peptides

A

Stimulate feeding behaviour - NPY and AgRP

30
Q

Anorexigenic Peptides

A

Decrease feeding behaviour - alpha-MSH and CART

31
Q

What is the MC4 (melanocortin 4) receptor?

A

Known to inhibit feeding behaviour. Both the orexigenic and anorexigenic peptides bind on the receptor.

32
Q

Agonist and Antagonist of MC4 receptor

A

Alpha MSH will act as an agonist

AgRP will act as an antagonist

33
Q

How is feeding inhibited by the MC4 receptor?

A

Increase in leptin after feeding = increased alpha MSH, decreased AgRP.
Alpha MSH will bind to MC4 receptor and inhibit feeding.

34
Q

What are the lateral hypothalamic peptides?

A

Melanin-concentrating hormone (MCH)

Orexin

35
Q

MCH

A
  • Widespread connections in the brain

- Prolongs consumption

36
Q

Orexin

A
  • Widespread cortical connections
  • Promotes meal initiatino
  • Also involved in wakefulness and arousal (plays a role in nacrolepsy, have low levels of orexin)
37
Q

Which anorexic peptides inhibit feeding behaviour and where are they found?

A

aMSH
CART
both from the arcuate nucleus

38
Q

Which orexigenic peptides stimulate feeding behaviour and where are they found?

A

NPY - arcuate nucleus
AgRP - arcuate nucleus
MCH - lateral hypothalamic area
Orexin - lateral hypothalamic area

39
Q

What happens when the regulation of food intake by the hypothalamus is disrupted?

A
  • Hyperphagia
  • Anorexia
  • Bulimia nervosa
40
Q

What are the three phases for short-term regulation of feeding?

A
  • Cephalic
  • Gastric
  • Substrate
41
Q

Describe the cephalic phase

A
  • Causes salivation and release of ghrelin when the stomach is empty.
  • This activates the NPY/AgRP-containing neurons in arcuate nucleus to stimulate feeding.
  • Removal of ghrelin - secreting cells of stomach thought to cause loss of appetite.
42
Q

Describe the gastric phase

A
  • Eating causes the distension of the stomach via the vagus nerve.
  • Works synergistically with CCK released in the intestines in response to certain foods.
  • Works to suppress feeding.
  • Insulin is also released by beta cells of the pancreas
43
Q

Connection between serotonin, food and mood.

A

5HT in the hypothalamus causes a rise in anticipation of food. Spike during a meal (especially carbohydrates in particular)

44
Q

What happens when eating chocolate?

A

High tryptophan in chocolate causing the production of serotonin as it is a precursor.

45
Q

What happens when there is low serotonin levels?

A

Associated anorexia nervosa, bulimia with depression.

46
Q

Why do we eat?

A
  • Hedonic aspect - like food, pleasurable effects of food - opioids
  • Drive reduction; wanting food as there is a distinction between liking and wanting, this is associated with dopaminergic system
47
Q

Natural rewards that could induce motivation

A
  • Food
  • Water
  • Sex
  • Nurturing
    Stimulates the positive feedback to allow us to do it again. This reinforces behaviour so it will be repeated. Each of these behaviours is required for the survival of the species.
48
Q

What do rewards activate?

A

The reward pathway of the mesolimbic system.

49
Q

What is the mesolimbic system?

A

Consists of dopaminergic neurons that project from the ventral tegmental area (VTA) to the nucleus accumbens.

50
Q

What is the function of the mesolimbic pathway?

A

Involved in motivation cognition and depletion of doapmine. It will decrease the extent an animal will go to obtain a reward.

51
Q

How was the mesolimbic pathway discovered?

A

When dopamin fluid levels were higher in the NA compared to the frontal cortex where no dopamine is released.

52
Q

Describe the mesolimbic pathway

A
  • VTA is connected to both the nucleus accumbens and the prefrontal cortex via this pathway and sends information to these structures via its neurons.
  • Dopamine is released in the nucleus accumbens and in the prefrontal cortex.
  • Important for the pleasuring and reward effect reinforcing the behaviour.
53
Q

How can drugs affect the reward system?

A

Drugs start to hijack the reward stimulate to hyper-stimulate it causing a greater release of dopamine. This will induce a large craving for the reward factor. This is a problem as it will increase the risk of dependence - continuing to do the rewarding behaviour.

54
Q

How does addiction occur?

A
  • After further administration of the drug, people tend to move to a pattern of escalating compulsive use due to tolerance and finally to dependence which is characterised by a state of emotional and physical withdrawal symptoms in short and sometimes long periods of abstinence.
  • Negative emotional state triggers the craving, the wanting of the drug that will drive the drug administration which is negative reinforcement.
55
Q

Define drug addiction

A

A chronic relapsing disorder characterised by compulsive seeking of the drug, loss of control over drug taking and emergence of negative emotional states and physical states when the drug is not provided.

56
Q

What induces drug intake?

A

Begins with social drug-taking during which the drug induces a hedonic, pleasureable effect which will trigger further drug administration. This is positive reinforcement.

57
Q

What is the switch in non-dependent and dependent drug users?

A

There is a transition from positive reinforcement to negative reinforcement driving drug intake.

58
Q

Positive reinforcement

A

Anything added that follows a behaviour that makes it more likely that the behaviour will occur again in the future.

59
Q

Negative reinforcement

A

A response or behaviour is strengthened by stopping, removing or avoiding a negative outcome or aversive stimulus.

60
Q

Summarise stages of addiction

A
  • A major motivational behaviour and occurs in stages.
  • Mainly started due to peer pressure, initial stages result in an increased feeling of reward.
  • Due to hyperstimulation of the reward system due to increased dopamine and high sense of reward individuals will take the drug again = positive reinforcement.
  • Addiction occurs when there is physical and emotional dependence due to withdrawal symptoms.
  • Taking the drug is usually an attempt of affected individuals to self-medicate in order to stop them from suffering from withdrawal symptoms.
61
Q

What is the difference in the brain in addicts compared to normal individuals?

A
  • D2 receptor levels are lower in a cocaine addicted person.
  • Decreased D2 means there is less reward which results in the craving in attempt to stimulate the D2 receptors.

Neuro (20 decks)

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