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Physiology 2 > Motivation > Flashcards

Motivation Flashcards

1
Q

What is motivation?

A
  • Driving force
  • Physical need
  • Wanting, liking
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2
Q

4 functions of the hypothalamus?

A
  1. A motivation controller
  2. Endocrine secretion
  3. Autonomic nervous system
  4. Emotions and drive behaviour
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3
Q

How do we load and empty the bodies energy reserves?

A

The nutrients are absorbed
The glucose goes to the liver and skeletal muscle where it is stored as glycogen - anabolism

A few hours later catabolism occurs and glycogen gets broken down to glucose

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4
Q

if Intake > expenditure, what is the term?

A

Obesity

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5
Q

If Intake < expenditure, what is the term?

A

starvation

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6
Q

What is Parabiosis?

A

Parabiosis: sharing of blood circulation between animals

Blood borne signals are shared and can affect the hypothalamus
A genetically obese mouse’s fat cells do not produce leptin (inhibitor of food intake)
Connected to a normal mouse will lead to a reduction of obesity in the ob/ob mouse

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7
Q

What does leptin do?

A

inhibiting food intake

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8
Q

What produces leptin and where does it act?

A
  • Fatty tissues produce leptin when satisfied

* Leptin travels to arcuate nucleus in brain to tell you to stop eating

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9
Q

Where is the hypothalamus and what does it contain?

A

The hypothalamus is at the base of the brain
Lining the third ventricle is the paraventricular and lateral hypothalamus
The arcuate nucleus

• Found under thalamus in the base of brain
• Adjacent to the third ventricle of brain
• Contains subhypothalmic nuclei (top to bottom)
o Paraventricle nucleus (where magnocellular projects from)
o Lateral hypothalamic area
o Ventromedial hypothalamus nuclei
o Arcuate nucleus (leptin receptor)

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10
Q

What is Lateral hypothalamus syndrome?

A

• Lateral hypothalamus syndrome: diminished appetite for food: anorexia

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11
Q

What is Ventromedial hypothalamic syndrome?

A

• Ventromedial hypothalamic syndrome: overeating and obesity (when VMH was leisioned)

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12
Q

Describe the anorexia response

A

After food intake leptin is increased in the circulation
It starts binding to the leptin receptors in the arcuate nucleus
Neurons in the arcuate nucleus get activated which project to the lateral hypothalamus
The neurons release Alpha MSH and CART peptides (anorectic peptides)
The peptides inhibit feeding behaviour
There is also stimulation of neurons that project to the paraventricular nucleus from the arcuate nucleus
This induces stimulation and release of ACTH and thyrotropin from the pituitary
This increases basal metabolic rate

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13
Q

Describe the Orexigenic response

A

Leptin levels are low
The CART and alpha MSH neurons are inhibited
Neurons in the arcuate nucleus get activated which project to the lateral hypothalamus
These neurons release NPY and AgRP
Projections from the arcuate nucleus to the paraventricular nucleus which inhibit release of ACTH and TSH
This decreases basal metabolic rate

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14
Q

Describe Competition for activation of MC4 receptor

A

Alpha MSH and the AgRP both act on bind to the same receptor MC4

Alpha MSH activates the receptor and inhibits feeding

AgRP inhibits the receptor and increases feeding

  • Anoretegenic alpha-MSH and orexigenic AgRP compete for MC4 receptor on neurone in lateral hypothalamic area.
  • Alpha-MSH stimulates it, AgRP inhibits
  • When activated feeding behaviour is inhibited
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15
Q

• LH neurones stimulating feeding behaviour contain:

A 
Melanin concentrating hormone (MCH) 
Widespread connections in the brain
Prolongs consumption
Orexin
Also with widespread cortical connections
Promotes meal initiation
Decreases sleep and increases arousal 
Promotes drug addiction
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16
Q

What is Satiety?

A
  1. Satiety is the feeling of fullness and the pression of hunger for a period of time after a meal
  2. Feelings of satiety can influence how soon and how much you next eat
  3. Feelings of satiety occurs due to the number of bodily signals that begin when food or drink is consumed and continues as it enters the gut and is digested and absorbed
17
Q

Describe the model for Model for short term regulation of feeding

A

Satiety signals rise in response to feeding
When high food consumption is inhibited
When satiety signals fall to zero, inhibition is eliminated, food consumption ensues

18
Q

What forms the satiety cascade?

A

There phases: cephalic, gastric, substrate (intestinal)

19
Q

Describe the cephalic phase of the satiety cascade

A

secretion of saliva
gastric juices secreted in the stomach in preparation for food
Activates NPY/AgRP
Removal of ghrelin-secreting cells

20
Q

Describe theI ntestinal and gastric phase of the satiety cascade

A

Release of ghrelin which acts on the brain

more secretion of saliva
more secretion of gastric juice
Distension signals via the vagus nerve
Works synergistically with CCK released in intestines in response to certain foods
Insulin also released by ß cells of the pancreas - important in anabolism

21
Q

Why do we eat?

A

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

Natural Rewards : food, water, sex, nurturing
They activate the reward system of the brain
This consists of dopaminergic neurons which project from the VTA to the nucleus accumbens
Addictive drugs are rewarding more than other reward inducing activities
If you take a mouse or a rat and you insert a probe in the nucleus accumbens and inject with amphetamine
There is a massive amount of dopamine released

When the mouse presses the lever it self-injects with cocaine
So the mouse keeps pressing the lever

22
Q

Describe Dopamine neurotransmission

A
  • Nucleus accumbens, when dopamine is at it, induces feeling of reward
  • Following amphetamines, major increase in dopamine release, so people get addicted
23
Q

What are the stages in addiction?

A

People usually take the drug in a social context
They take it due to the pleasurable effect
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

The dose will increase due to tolerance and this leads to dependent
They suffer from physical and emotional withdrawal symptoms when the drug is taken away
They then take the drug in an attempt to self-medicate to make the symptoms go away

24
Q

What is positive and negative reinforcement?

A
  • Positive reinforcement (anything added that follows a behavior that makes it more likely that the behavior will occur again in the future)
  • Negative reinforcement (a response or behavior is strengthened by stopping, removing or avoiding a negative outcome or aversive stimulus)
25
Q

What roles do D2 receptors play in obesity?

A
  • Decrease of D2 dopamine receptors is a biomarker of addiction: they eat/ take more drugs to try to simulate the same way
  • Hippocampus-associated with memory, implemented is memory of food or drug is strong especially in people with dependence
  • Amygdala-associated with emotionality drug dependant individuals how a strong emotional connection to the drug

People who suffer from addiction have their reward systems suppressed
The receptor can be detected with PET
Inject someone wit h a radiotracer which is selective for the D2 receptors
Wanting is driven by dopamine
The hedonic effect (liking things) that drives motivation behaviour is driven by the opioid system such as endorphins

26
Q

What is Operant behaviour?

A
  • Rat is placed in box with lever
  • When pushes lever gives rat ad drug and stimulates reward
  • Rat will keep pushing lever to get more reward
27
Q

What is Microdialysis?

A
  • Measuring neurotransmitter release in vivo

* Association with behaviour parameters

28
Q

What does dopamine release into the NA cause?

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
29
Q

What does a rise in 5-HT in the hypothalamus cause?

A

 Rises in anticipation of food
 Spike during a meal (carbohydrates in particular)
 Association anorexia nervosa, bulimia with depression (low serotonin)

Physiology 2 (36 decks)

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