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(Anna) NEUR30003 - Principles of Neuroscience > Lecture 18- Motivation > Flashcards

Lecture 18- Motivation Flashcards

1
Q

What does behaviour (motor activation) occur in response to?

A

1.Reflex stimulation- dropping a hot object= automatic 2.Conscious or willful command (motivated behaviour)

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2
Q

What does motivated behaviour occur in response to?

A

-response to body’s absolute requirements (eating when hungry) -or by abstract things (reading a book) -motivation= driving force on behaviour

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3
Q

What is energy balance an example of?

A
  • example of tightly controlled homeostatic process -go up and down bodyweight but mostly stable -can take away food= still stay the same weight for a bit, then drops -give food again= body weight goes to normal -force feed the animal= heavier, then stop and comes back to normal -set point of body weight= the one the body wants
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4
Q

What is the lipostatic hypothesis?

A

-it is the fat that is being monitored in a body to maintain body weight

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5
Q

What part of the brain is key in lipstatic homeostasis?

A

hypothalamus is key in this

  • 3 nuclei
  • paraventricular nucleus
  • lateral hypothalamic area
  • arcuate nucleus

(disruption in these 3 nuclei= big change in bodyweight)

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6
Q

What happens when you have a lesion of lateral hypothalamus?

A
  • lateral hypothalamic syndrome
  • get really skinny
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7
Q

What happens when you have a lesion of ventromedial hypothalamus?

A
  • ventromedial hypothalamic syndrome
  • get fat
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8
Q

What is between your scapuli?

A

-brown adipose tissue -storgage -receives sympathetic innervation -when gets a signal undergoes process where it burns energy and makes heat -because it is peripheral the heat is lost -so wasting the energy -this is a way very thin people who don’t exercise stay thin

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9
Q

What are the neurons involved in the energy control of the body (brown tissue)?

A
  • in arcuate nucleus, two types of neurons that are key in the process
  • 1.neuropeptide y (makes it) so the name of it is this
  • 2.agouti related peptide
  • 3.POMC (propiomelanocortin) neuron
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10
Q

What do the AgRP and NPY cause?

A

-release of these peptides will increase food intake (The Agouti related peptide and neuro peptide Y), decrease energy expenditure (less activity of the brown adipose tissue)

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11
Q

What does the POMC cause?

A

produces= , peptide called alpha alphaMSH (alpha melanocyte stimulating hormone)= that is the important =inhibits food intake and increases energy expenditure (more active brown adipose tissue)

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12
Q

What is in the arcuate nucleus?

A

-energy intake stimulating and inhibiting neurons, then go to second order neurons to modulate behaviour

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13
Q

What is the interaction of alphaMSH and AgRP?

A
  • POMC neuron release sits ligand: alpha MSH stimulates the MC4 receptor (eg. lateral thalamus) to inhibit feeding behaviour
  • AgRP is being released from the other class of neurons= it is a functional antagonist of alpha MSH, binds to the same receptor
  • blocking the alpha MSH from binding
  • NPY acts through a different receptor (so the AgRP inhibits alpha MSH and NPY activates sth)
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14
Q

Which receptor do AgRP and alphaMSH act through?

A

MC4

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15
Q

Where do the alphaMSHT neurons project to?

A

–to lateral hypothalamic area where the inhibit feeding behaviour

  • to paraventricular nucleus= these do two things
    1: stimulate release of ACTH (mobilizes energy stores)
    2: activate sympathetic outflows to affects the brown adipose tissue= so expend more energy
  • bring bodyweight down
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16
Q

Where do the NPY and AgRP neurons project to?

A
  • project to lateral hypothalamic area= stimulate feeding behaviour
  • then to paraventricular nucleus where they inhibit secretion of ACTH = less heat from brown fat
  • decrease loss of energy and increase feeding = body weight goes up!
17
Q

What is lateral hypothalamus critical for?

A

-regulation of food intake (and other homeostatic behaviour associated with body weight regulation)

18
Q

What innervation do the lateral hypothalamic neurons receive?

A

-both stimulatory and inhibitory inputs from leptin-sensitive neurons of the arcuate nucleus

19
Q

What are the two main groups of neurons of the lateral hypothalamic area that are involved in food intake?

A

-orexin containing= arousal(more active) -melanin-concentrating hormone containing

20
Q

What is leptin and its effect?

A

= hormone made and released from adipose tissue -more adipose tissue= more leptin -comes up to the arcuate nucleus,where leaky blood brain barrier so the leptin can affect the neurons -decrease food intake and increase expenditure of energy -inhibits AgRP and NPY and stimulates the POMC neurons

21
Q

What substances feed into the arcuate nucleus?

A
  • insulin, leptin and some nutrients(free fatty acids)
  • they inhibit the AgRP/NPY and stimulate POMC
22
Q

What is the story with the Ob/ob mouse?

A

-genetic mutation= ob/ ob mouse= really obese -joined a normal mouse to an ob ob mouse via a skin graft (parabiosis) -genetically identical -connected= share blood supply so something in the blood supply must cause the dirfference -then both mice of normal body weight

23
Q

What restores normal weight in Ob/Ob mice?

A

-infusion of leptin -leptin acts via the neurons in the arcuate to regulate lipid homeostasis -the more fat the more leptin you have

24
Q

Why can we get fat? (leptin)

A

-get insensitive to leptin

25
Q

What does leptin do?

A

–leptin stimulates the alpha MSH -leptin inhibits AgRP

26
Q

Where is leptin produced?

A

-by the adipose tissue and acts as a signal to decrease food intake (leptin deficiency leads to obesity)

27
Q

What doe leptin act via?

A

-the arcuate nucleus in the basal hypothalamus

28
Q

What does leptin stimulate?

A

-neurons containing the alphaMSH which acts via specific receptors (MCR3/4) in the lateral hypothalamus to decrease food intake

29
Q

What does leptin inhibit?

A

-population of neurons in the arcuate nucleus that contain the peptide neuropeptide Y (NPY) which also acts via specific receptors in the lateral hypothalamus to stimulate food intake

30
Q

What is the main effect of leptin?

A

-decrease in food intake

31
Q

What is the db/db mouse?

A

-dbdb mouse also obese= has a defect in leptin receptor and eventhough leptin is produced but it doesn’t do its job

32
Q

What is the long term regulation of energy balance?

A

-leptin as measure of adiposity

33
Q

What is the short term regulation of energy balance?

A

-food intake triggers satiety signals 1.Gastric distension(vagus nerve to hindbrain) 2.Cholecystokinin(vagus nerve to hindbrain) 3.Insulin (directly to basal hypothalamus) -increase insulin together with increased glucose is a powerful satiety signal

34
Q

What stimulates food intake?

A

-many factors, one is decrease in blood glucose

35
Q

Which part of the brain is involved in the food reward system?

A
  • basal forebrain area
  • ventral tegmental area

—we eat because we need the energy but also like to eat -food intake activates the reward pathway

36
Q

What drugs are in the reward pathway?

A

-dopamine, heroin and nicotine work on the dopamiinergic neurons =part of the reward system

37
Q

What is the CB1 receptor?

A

CB1 is the receptor binding the active ingredient in marihuana = munchies -in brain have endocanabinoids that act on the reward thing -that is why the marihuana can act on it = highjacking -we stopped antacannaboids action -helps with body weight loss -the antacannaboids= have effect on perception

38
Q

What happens to serotonin when we see or smell food?

A

-increases!

39
Q

How is energy stored in the body?

A
  1. glycogen gets stored in energy and muscles, there is a limited capacity to store glycogen in the body
  2. other group are triglycerides, thesed get stored in adipose tissue, there is virtually limitless amount of it that can be stored -glucose, fatty acids and ketones can be used directly for energy, glucose essential for neurons

(Anna) NEUR30003 - Principles of Neuroscience (35 decks)

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