Lecture 18- Motivation Flashcards Preview

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Flashcards in Lecture 18- Motivation Deck (39):

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

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


What does motivated behaviour occur in response to?

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


What is energy balance an example of?

- 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


What is the lipostatic hypothesis?

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


What part of the brain is key in lipstatic homeostasis?

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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What happens when you have a lesion of lateral hypothalamus?

-lateral hypothalamic syndrome

-get really skinny

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What happens when you have a lesion of ventromedial hypothalamus?

-ventromedial hypothalamic syndrome

-get fat

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What is between your scapuli?

-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


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

-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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What do the AgRP and NPY cause?

-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)


What does the POMC cause?

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)


What is in the arcuate nucleus?

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


What is the interaction of alphaMSH and AgRP?

-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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Which receptor do AgRP and alphaMSH act through?



Where do the alphaMSHT neurons project to?

--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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Where do the NPY and AgRP neurons project to?

-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!

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What is lateral hypothalamus critical for?

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


What innervation do the lateral hypothalamic neurons receive?

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


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

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


What is leptin and its effect?

= 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


What substances feed into the arcuate nucleus?

-insulin, leptin and some nutrients(free fatty acids)

-they inhibit the AgRP/NPY and stimulate POMC

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What is the story with the Ob/ob mouse?

-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


What restores normal weight in Ob/Ob mice?

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


Why can we get fat? (leptin)

-get insensitive to leptin


What does leptin do?

--leptin stimulates the alpha MSH -leptin inhibits AgRP


Where is leptin produced?

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


What doe leptin act via?

-the arcuate nucleus in the basal hypothalamus


What does leptin stimulate?

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


What does leptin inhibit?

-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


What is the main effect of leptin?

-decrease in food intake


What is the db/db mouse?

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


What is the long term regulation of energy balance?

-leptin as measure of adiposity


What is the short term regulation of energy balance?

-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


What stimulates food intake?

-many factors, one is decrease in blood glucose


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

-basal forebrain area

-ventral tegmental area

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

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What drugs are in the reward pathway?

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

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What is the CB1 receptor?

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


What happens to serotonin when we see or smell food?



How is energy stored in the body?

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