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Neurology > Motivation > Flashcards

Motivation Flashcards

1
Q

What is motivation?

A

Driving force
Physical need
Wanting, liking

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2
Q

How odes the hypothalamus regulate motivation?

A

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

What happens to the energy taken in by our food?

A

Energy from food is broken down to be taken up by cells. Any excess is stored as glycogen in the liver and muscles. Triglycerides are stored in adipose tissue

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4
Q

Explain how energy is released during periods of starvation

A

During periods of starvation, glycogen is broken down into glucose
In both, anabolic and metabolic reactions are tightly regulated.

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5
Q

How is feeding behaviour regulated long term?

A

Normal energy balance leads to normal adiposity

Prolonged positive energy balance leads to obesity

Prolonged negative energy balance leads to starvation

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6
Q

How does the hypothalamus regulate homeostasis?

A

Transduction of physiological stimuli in blood in specialized region of hypothalamus

Humoral and visceromotor responses are initiated by activation periventricular and medial hypothalamus

Behavioural action depends on lateral hypothalamus

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7
Q

How is body weight regulated around a set value?

A

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 is rapidly gained when food is freely available

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8
Q

What is parabiosis?

A

sharing of blood circulation between animals.

Blood borne signals are shared and can affect the hypothalamus.

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9
Q

Which hypothalamic nucleus regulates feeding?

A

Arcuate Nucleus: important for control of feeding (effect of leptin on arcuate nucleus)

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10
Q

Describe the role of the arcuate nucleus in regulating feeding

A

After feeding, fat adipose tissues get replenished and release leptin into the blood circulation.

Leptin binds to its receptors in the arcuate nucleus (hypothalamus) signalling to the brain to stop eating - ‘full sensation’

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11
Q

What is the significance of the VMH and Lateral hypothalamus?

A

Important for the regulation of

  • Body weight/food intake
  • Blood volume/osmolarity: drinking
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12
Q

Where is the hypothalamus located?

A

Hypothalamus located under the thalamus at the base of the brain

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13
Q

Where in the hypothalamus is the arcuate nucleus found?

A

At the bottom part of the third ventricle is where the arcuate nucleus is found

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14
Q

Describe the location of other hypothalamic nuclei

A

The paraventricular nuclei is adjacent to the third ventricle and below it is the lateral hypothalamus area

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15
Q

How was the significance of VMH proved?

A

VMH lesion caused excessive eating to the point where the mouse became obese - showing the ventral medial hypothalamus is crucial in regulating body weight

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16
Q

What is the consequence of VMH lesion?

A

VMH plays a role in controlling the cessation of eating

Damage to the VMH results in prolonged and dramatic weight gain

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17
Q

What are the effects of lesions to the VMH and LH?

A

Lateral hypothalamic syndrome: diminished appetite for food; anorexia

Ventromedial hypothalamic syndrome: overeating and obesity
Both related to leptin signaling

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18
Q

What is the effect of elevated leptin levels?

A

Anorexic response

Rise in leptin levels in blood is detected by arcuate nucleus neurons that contain the peptides 𝜶MSH and CART
These neurons project axons to the lower brainstem and spinal cord, paraventricular nucleus of the hypothalamus, and inhibit the lateral hypothalamus

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19
Q

What is the role of the projections to the LH?

A

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

20
Q

What is the result of decreased leptin levels?

A

Orixegenic response

Reduction on blood levels of leptin detected by arcuate nucleus neurons containing peptides NPY and AgRP
These arcuate nucleus neurons inhibit paraventricular nuclei controlling release of TSH and ACTH from pituitary (via 𝜶MSH and CART)

They activate neurons in lateral hypothalamus that stimulate feeding behaviour
Some of the activated lateral hypothalamic neurons contain the peptide MCH (melanin-concentrating hormone)

21
Q

Describe the competition for the MC4R

A

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

22
Q

Describe how leptin levels effect MC4R competition

A

When you’ve eaten well there is increased leptin in blood circulation causing an increase in 𝜶MSH and decrease AgRP stimulation. 𝜶MSH then binds to MC4R to inhibit feeding

23
Q

How is the MC4R activated?

A

While 𝜶MSH (agonist) stimulates the MC4 receptor, AgRP (antagonist) inhibits it

24
Q

What are the 2 other factors contained in LH neurons that stimulate feeding?

A
  • Melanin-concentrating hormone (MCH)

- Orexin

25
Q

Describe the effects of MCH

A

Widespread connections in the brain

Prolongs consumption

26
Q

Describe the effects of orexin

A

Also with widespread cortical connections

Promotes meal initiation

27
Q

What are the consequences of disruption to the hypothalamic control of body weight and food intake?

A

Disruption of this regulation leads to

  • Hyperphagia
  • Anorexia
  • Bulimia nervosa
28
Q

What are the 3 phases of feeding?

A

Three phases: cephalic, gastric, substrate

29
Q

How do satiety signals control feeding behaviour?

A

Satiety signals rise in response to feeding
When satiety signals are high, food consumption is inhibited (full feeling).

When the satiety signals falls to zero the inhibition is eliminated and food consumption ensues

30
Q

Outline what occurs during satiation

A

Sight of food (before eating)
PNS and enteric activation
Saliva & Digestive juices secretion

Much more intense secretions when chewing / swallowing

31
Q

Describe the events of the cephalic phase

A

Cephalic: hunger
- Ghrelin released when stomach is empty
- Activates NPY/AgRP-containing neurons in the arcuate
nucleus
- Removal of ghrelin-secreting cells of stomach thought to
cause loss of appetite

32
Q

What occurs during the gastric phase of feeding?

A

Gastric: feeling full
- Gastric distension signals brain via the vagus nerve.
- Works synergistically with CCK released in intestines in
response to certain foods
- Insulin also released by β cells of the pancreas—
important in anabolism

33
Q

Describe the effects of satiety

A

CCK released by intestine in response to fatty food
Acts on vagus nerve to inhibit feeding
Insulin is a satiety signal

34
Q

What is the effect of serotonin on food intake?

A

Mood and food are connected
5HT in hypothalamus
- Rises in anticipation of food
- Spike during a meal (carbohydrates in particular)
- Association anorexia nervosa, bulimia with depression (low serotonin)

35
Q

Why do we eat?

A

We like food - Hedonic aspect
We want food - Drive reduction
Liking and wanting mediated in part by separate brain circuits
Dopaminergic system involved in wanting/ craving (or liking?)

36
Q

What are natural rewards?

A 
Food 
Water
Sex 
Nurturing 
Social interactions
37
Q

Describe the reward system of the brain

A

These natural rewards activate the mesolimbic system - reward pathway of the brain

This consists of dopaminergic neurons that project from the VTA to the nucleus accumbens where dopamine is released

38
Q

How does addiction occur?

A

Addictive drugs act on the dopaminergic pathways from the ventral tegmental area to the nucleus accumbens

39
Q

Describe how someone gets addicted

A

After the initial stages of addiction you start getting rewards making you want to do it again = positive reinforcement behaviour
Increased activation of the mesolimbic pathway

40
Q

How does someone become dependent on an addiction?

A

Continuation causes some people to become dependent on drugs - withdrawal symptoms and behaviours prevail both physical and psychological

At this stage the addict is no longer taking the drugs to get high but to self medicate and put off the withdrawal symptoms

41
Q

What is positive reinforcement?

A

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

42
Q

What is negative reinforcement?

A

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

43
Q

How is D2 receptor presence different in addiction patients?

A

D2 receptor decrease in addicted individuals causing lower levels of rewards - the drug they’re addicted to is used in an attempt to stimulate those reward centres

44
Q

What is the significance of the amygdala?

A

Amygdala is the emotional centre of the brain also involved in the motivational regulation along with the mesolimbic pathway

45
Q

What is microdialysis?

A

Measuring neurotransmitter release in vivo

Association with behaviour parameters

46
Q

Describe the role of dopamine in motivating behaviours

A

Dopamine release in the nucleus accumbens is correlated with motivation but not liking (hedonic)
Its also release in anticipation of reward
Note that dopamine also involved in movement

47
Q

What other regions work alongside the hypothalamus in motivation regulation?

A

There is a strong connectivity between the hypothalamus and the periphery (e.g. leptin and ghrelin release)
There are also projections from the hypothalamus to other brain regions such as reward centres of the brain, emotional centre (amygdala) as well as cognitive centres

Neurology (20 decks)

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