Neuro: Motivation Flashcards

1
Q

What is motivation?

A

Motivation is a driving force driven by either a physical need or the wanting/liking of something

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2
Q

Briefly explain process of anabolism

A
  • After eating absorbed nutrients from food enter bloodstream and get converted into glucose, ketones and fatty acids which provide energy to the cells of body
  • Excess absorbed nutrients get converted into triglycerides which get stored as adipose tissue
  • They also get converted into glycogen which get stored in liver and skeletal muscle
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3
Q

Briefly explain process of catabolism

A
  • During period of starvation triglycerides in adipose tissue get broken down to glucose, ketones and fatty acids
  • Glycogen in liver and gets broken down into glucose
  • These substances provide energy to cells of body
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4
Q

How do we know that bodyweight is regulated?

A
  • If you put an animal through a period of starvation it will lose weight
  • If you then re-introduce that animal to a normal diet it will then gain weight until its bodyweight goes back to the level it was before the level of starvation
  • If you put an animal through a a period of force-feeding it will gain weight
  • If you then put it back onto a normal diet it lose weight until its body weight goes to back to pre-force feeding levels
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5
Q

Explain how the parabiosis experiment proved that hormones in the blood are able to regulate bodyweight

A
  • Parabiosis: sharing of blood circulation between animals
  • Experiment involved connecting obese mouse, with no copies of ob gene, with normal mouse, which had 2 copies of ob gene.
  • Normal and obese mice shared blood circulation and leptin produced from expression of ob gene of normal mouse was able to effect hypothalamus of obese mouse as well
  • Obese mouse couldn’t produce leptin before as it didn’t have ob gene
  • Production of Leptin meant obese mouse losing bodyweight
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6
Q

Briefly explain the feedback leptin produces on the brain to cause someone to stop eating

A
  • After feeding adipose tissue reserves get replenished due to conversion of nutrients into triglycerides
  • When adipose tissue gets replenished it secretes leptin into the bloodstream
  • Leptin travels to arcuate nucleus of hypothalamus and binds to leptin receptors
  • This tells the brain that person is full and causes them to stop eating
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7
Q

Where specifically within the brain is the arcuate nucleus found?

A
  • It’s found in the hypothalamus
  • Specifically it’s found at the bottom of the third ventricle of the brain
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8
Q

Apart from the arcuate nuclei what other nuclei are found surronding the third ventricle of the brain?

A
  • On either side of the third ventricle there’s a nucleus called the paraventricular nucleus
  • Directly underneath both paraventricular nuclei is the lateral hypothalamus
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9
Q

What happens to the body weight of a mouse in which its ventromedial hypothalamus is lesioned? What does this show?

A
  • Body weight increased massively
  • This shows ventromedial hypothalamus important for preventing too much weight gain
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10
Q

What happens to the body weight of a mouse in which its lateral hypothalamus is lesioned? What does this show?

A
  • Body weight reduced dramatically
  • This shows lateral hypothalamus important for preventing too much weight reduction
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11
Q

Explain how elevated leptin levels in the body cause inhibition of feeding behaviour (stop eating)?

A
  • Leptin binds to leptin receptors on arcuate nucleus leading to activation of arcuate neurons
  • Activated arcuate neurons release αMSH and CART peptides
  • Arcuate nucleus neurons project to the lateral hypothalamus so release of αMSH and CART peptides leads to inhibition of lateral hypothalamus
  • Inhibition of lateral hypothalamus inhibits feeding
  • Release of αMSH and CART peptides from activated arcuate nucles neurons also leads to activation of paraventricular nucleus
  • This leads to release of ACTH and TSH from anterior pituitary which causes big increase in metabolism
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12
Q

What is the collective term for αMSH and CART peptides?

A

Anorectic peptides

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13
Q

Explain how reduced leptin levels lead to stimulation of feeding behaviour (start eating)?

A
  • In response to low levels of leptin neurons of the arcuate nucleus that secrete NPY and AgRP become activated
  • Secretion of NPY and AgRP peptides from these neurons leads to activation of lateral hypothalamus
  • Activation of lateral hypothalamus stimulates feeding behaviour
  • Low leptin levels also leads to inhibition of paraventricular nucleus via neurons that project to it from arcuate nucleus
  • Inhibition of paraventricular nucleus inhibits release of ACTH and TSH from anterior pituitary
  • This leads to decrease in metabolism
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14
Q

What is the collective term for the NPY and AgRP peptides?

A

Orexigenic peptides

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15
Q

What is the name of the receptor on the lateral hypothalamus that both αMSH and AgRP bind to?

A

MC4 recptor

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16
Q

What effect do αMSH and AgRP have on the MC4 receptor?

A
  • αMSH is an agonist and so activates MC4 receptor
  • AgRP is an antagonist and so inhibits the MC4 receptor
17
Q

Apart from the anorectic and orexigenic peptides released from the arcuate nucleus what other peptides can affect feeding behaviour? Where are the released from?

A
  • Melanin-concentrating hormone (MCH)
  • Orexin
  • Both released from neurons of lateral hypothalamus
18
Q

What effect do MCH and orexin have on feeding behaviour?

A
  • Melanin-concentrating hormone (MCH) - prolongs food consumption so increases feeding behaviour
  • Orexin - Promotes meal initiation so increases feeding behaviour
19
Q

As well as the long-term regulation of feeding provided by the hypothalamus there is also short-term regulation of feeding (satiety or feeling full) What are the 3 stages of satiety?

A
  • Cephalic phase
  • Gastric phase
  • Substrate phase
20
Q

What occurs during the cephalic phase of satiety?

A
  • Increased saliva and gastric secretions
  • Increased secretion of ghrelin from stomach
21
Q

Explain the effect ghrelin release has on feeding

A
  • Ghrelin release from stomach causes secretion of NPY and AgRP from neurons in the arcuate nucleus
  • This leads to activation of lateral hypothalamus leading to stimulation of feeding behaviour
22
Q

What occurs during the gastric phase of satiety?

A
  • Eating leads to gastric distention
  • Gastric distention leads to activation of the vagus nerve
  • Activated vagus nerve sends signals to nucleus of the solitary tract which causes you to stop eating
  • CCK is also released from the gut and also activates vagus nerve
23
Q

What happens to serotonin levels in the hypothalamus before and during feeding?

A
  • 5-HT (Serotonin) release into hypothalamus rises in anticipation of food
  • Then during a meal there’s a spike in serotonin release
24
Q

How is mood associated with food and feeding?

A
  • Disorders connected to eating such as anorexia nervosa and bulimia are associated with depression with one of the causes of depression being low serotonin levels
25
Why do we eat even when we aren't hungry?
* We like food - eating food is pleasureable * We want food - motivational drive to go get food
26
Name some natural rewards
* Food * Sex * Water * Nuturing
27
What pathway of the brain do rewards activate?
Mesolimbic pathway - from ventral tegmental area (VTA) to the nucleus accumbens and then frontal cortex
28
Explain how release of dopamine due to a drug results in addiction to that drug
* Addictive drugs hyperstimulate mesolimbic pathay to cause massive release of dopamine from ventral tegmental area into nucleus accumbens and pre-frontal cortex * This causes massive high/makes you feel good * After that experience you remeber the high so you get increased motivation to feel the same high again which leads to repeat use * Eventually repeat use leads to a person needing more of a drug to feel same high * This leads to dependence
29
During later stages of addiction the motivation for someone taking a drug changes. What is this change of motivation?
* When someone is addicted to drug and they don't take it for a particular length of time they experience withdrawal symptoms * At this point in addiction motivation for somebody taking the drug changes from wanting to feel the high it caused to just trying to offset the withdrawal symptoms
30
What is positive reinforcement?
When a desirable stimulus is presented as a consequence of a behavior and the chance that this behavior will manifest in similar environments increases
31
What is negative reinforcement?
When a response or behavior is strengthened by stopping, removing or avoiding a negative outcome or aversive stimulus