NEURO: Motivation Flashcards

1
Q

What is motivation?

A

Motivation is an urge to behave or act in a way that will satisfy certain conditions, such as wishes, desires, or goals.

It is a driving force to fulfil biological needs.

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2
Q

What is the function of the hypothalamus?

A

Its function is to maintain homeostasis by regulating three interrelated functions:

  • endocrine secretion
  • autonomic nervous system
  • emotions and drive/behaviour (motivated behaviour, e.g. drinking, eating)
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3
Q

Describe the long-term effects of feeding behaviour.

A

Normal energy balance leads to normal adiposity.

Prolonged positive energy balance leads to obesity.
Prolonged negative energy balance leads to starvation.

Body weight is normally stable. If an animal is force-fed, it will gain weight, The weight is lost, however, as soon as the animal can regulate its own food intake. Similarly, weight lost during a period of starvation if rapidly gained when good is freely available.

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4
Q

List some principles of the hypothalamus, homeostasis and motivated behaviours.

A
  • transduction of physiological stimuli in blood in a specialized region of hypothalamus
  • humoral and visceromotor responses are initiated by activation of the periventricular and medial hypothalamus
  • behavioural action depends on the lateral hypothalamus
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5
Q

Give an example of the effects of parabiosis on the body weight of ob/ob mice.

A

Parabiosis is the sharing of blood circulation between animals. This means the blood borne signals are shared and can affect the hypothalamus.

Example 1:
A genetically obese mouse (ob/ob) means that its fat cells do not produce leptin (which inhibits food intake).
It’s connected to a normal mouse (which produces leptin), and this lead to a reduction of obesity in the ob/ob mouse .

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6
Q

Describe the leptin feedback.

A

When there is increased fatty tissue, it produces leptin when it is ‘satisfied’.

The leptin travels to the brain to tell you to stop eating (by acting on the arcuate nucleus).

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7
Q

What are the ventromedial and lateral hypothalamus important for?

A

It’s important for the regulation of:

  • body weight/food intake
  • blood volume/osmolarity: drinking
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8
Q

What was the conclusion of a VMH lesion?

A

It concludes that the VMH plays a role in the cessation of eating. Damage to the VMH results in prolonged and dramatic weight gain.

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9
Q

What results from a lateral hypothalamus syndrome?

A

You get diminished appetite for food, which can result in anorexia.

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10
Q

What is the arcuate nucleus’s response to elevated leptin levels?

A

A rise in leptin levels in the blood is detected by neurons in the arcuate nucleus that contain the peptides αMSH and CART. These are anorectic peptides which diminish appetite.
These neurons project axons to the lower brain stem and spinal cord, the paraventricular nuclei of the hypothalamus, and the lateral hypothalamic area.

Each of these connections contributes to the coordinated humoural, visceromotor, and somatic motor responses to increased leptin levels.

This is known as an anorexic response.

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11
Q

What is the arcuate nucleus’s response to decreased leptin levels?

A

A reduction in blood levels of leptin is detected by neurones in the arcuate nucleus that contain peptides NPY and AgRP. These arcuate nucleus neurones inhibit the neurons in the paraventricular nuclei that control the release of ACTH and TSH from the pituitary.

In addition, they activate the neurons in the lateral hypothalamus that stimulates feeding behaviour. Some of the activated lateral hypothalamic neurons contain the peptide MCH (melanin-conncentrating hormone).

This is known as an orexigenic response.

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12
Q

Describe the competition for activation of the MC4 receptor?

A

One way that αMSH (an anorectic peptide) and AgRP (an prexigenic peptide) exert opposite effects on metabolism and feeding behaviour is via an interaction with the MC4 receptor on some hypothalamic neurons.

While αMSH stimulates the MC4 receptor, AgRP inhibits it. Stimulation of the MC4 receptor inhibits feeding behaviour.

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13
Q

What do the LH neurons that stimulate feeding behaviour contain?

A

Melanin-concentrating hormone (MCH):

  • has widespread connections in the brain
  • prolongs consumption

Orexin

  • also has widespread cortical connections
  • promotes meal initiation
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14
Q

Describe the hypothetical model for short-term regulation of feeding.

A

A possible means of regulating food consumption is by satiety signals.

Satiety signals rise in response to feeding. When satiety signals are high, food consumption is inhibited. When the satiety signals fall to zero, food consumption ensues.

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15
Q

What happens during the cephalic phase?

A

This is the hunger phase.

  • ghrelin is released when the stomach is empty
  • it activates NPY/AgRP-containing neurons in the arcuate nucleus
  • there is the removal of ghrelin-secreting cells of stomach, which is thought to cause loss of appetite
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16
Q

What happens during the gastric phase?

A

This is the feeling full stage.

  • gastric distension signals brain via the vagus nerve
  • it works synergistically with CCK released in the intestines in response to certain foods
  • insulin is also released by β cells of the pancreas (important in anabolism)
17
Q

How is mood connected to food?

A

5HT in hypothalamus:

  • rises in anticipation of food
  • spikes during a meal (with carbohydrates in particular)
  • has an association with anorexia nervosa, bulimia with depression (low serotonin)
18
Q

Why do we eat?

A

We eat because of the natural reward system. When we bite into our food, we get a release of tryptophan, a precursor for serotonin. Thus, we want to eat food again.

19
Q

Describe the reward pathway.

A

The ventral tegmental area (VTA) is connected to both the nucleus accumbens and the prefrontal cortex via this pathway, and it sends information to these structures via its neurones.

The neurones of the VTA contain dopamine, which is released in the nucleus accumbens and in the prefrontal cortex. This pathway is activated by a rewarding stimulus.

20
Q

What is drug addiction?

A

Drug addiction is defined as a chronic relapsing disorder characterised by compulsive seeking of the drug, loss of control over drug taking and emergence of negative emotional states (anxiety, dysohoria, irritability) and physical states when the drug is not provided (withdrawal symptoms).

21
Q

Describe the stages in the addiction cycle.

A

Drug intake begins with social drug-taking during which the drug induces a hedonic, pleasurable effect which will trigger further drug administration. This is called positive reinforcement: when drug taking is triggered by the positive, pleasurable effects of the drug, which is a process also triggered by natural rewards.

The mesolimbic dopaminergic system, which consists of dopaminergic neurons projecting from the VTA to the Nacb, have long been considered the major neurobiological substrates mediating all drugs positive reinforcement (including alcohol, opioids, canabis, nicotine. They all induce dopamine release in the nucleus accumbens.

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 (anxiety, depression etc.) in short and sometimes long periods of abstinence.

Now, this negative emotional state triggers the craving, the wanting of the drug which will drive the drug administration which is called negative reinforcement. In other words the aversive, dysphoria experience of drug withdrawal drives now the drug intake, NOT the positive hedonic property of the drug. Regions of the extended amygdala such as the amygdala, hypothalamus, hippocampus as well as the nucleus accumbens and release of NA, CRF, GABA are known to be involved in the aversive negative reinforcement in dependent people.

There is a basically a transition from positive reinforcement in non dependent people to negative reinforcement in dependent people which drives the drug intake. Relapse is very likely in the withdrawal period (induced by the drug itself, stressors, cues), and therefore the cycle is repeated.

22
Q

What is the difference between positive and negative reinforcement?

A

Positive reinforcement: anything added that follows a behaviour that makes it more likely that the behaviour will occur again in the future.

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

23
Q

What is microdialysis?

A

It’s the measuring of neurotransmitter release in vivo.

It has an association with behaviour parameters.

24
Q

How is dopamine related to reinforcement?

A

Dopamine release in the nucleus accumbens is correlated with motivation but not liking (hedonic).

Its also released in anticipation of reward.
[note that dopamine also involved in movement]