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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the collective term for αMSH and CART peptides?

A

Anorectic peptides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A

Orexigenic peptides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

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

A

MC4 recptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

Why do we eat even when we aren’t hungry?

A
  • We like food - eating food is pleasureable
  • We want food - motivational drive to go get food
26
Q

Name some natural rewards

A
  • Food
  • Sex
  • Water
  • Nuturing
27
Q

What pathway of the brain do rewards activate?

A

Mesolimbic pathway - from ventral tegmental area (VTA) to the nucleus accumbens and then frontal cortex

28
Q

Explain how release of dopamine due to a drug results in addiction to that drug

A
  • 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
Q

During later stages of addiction the motivation for someone taking a drug changes. What is this change of motivation?

A
  • 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
Q

What is positive reinforcement?

A

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
Q

What is negative reinforcement?

A

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