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A Intro to Neuro > Motivation & Homeostasis > Flashcards

Motivation & Homeostasis Flashcards

1
Q

Overview of homeostasis

A
  • Goal of eating, drinking, and staying warm is to maintain balance/equilibrium within internal environment, even in the face of external changes
  • Keep certain physiological variables in a fixed range (also called defined range, optimal range, or set point (in the case of very narrow ranges))
  • Feedback is used to bring deviations of a variable back to a set point
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2
Q

Role of the hypothalamus in homeostasis

A
  • A parameter (e.g. temperature) is measured by specialized sensory neurons
  • Deviations from set point are detected by neurons in periventricular zone (PVZ) of hypothalamus
  • PVZ neurons mount an integrated response to bring parameter back to optimal range
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3
Q

What are the three components of homeostasis by the hypothalamus?

A
  • Humoral
  • Visceromotor
  • Somatic motor
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4
Q

Humoral component of hypothalamus homeostasis

A

Stimulating or inhibiting release of pituitary hormones into bloodstream

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5
Q

Visceromotor component of hypothalamus homeostasis

A

Adjust balance of sympathetic and parasympathetic outputs in the ANS

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6
Q

Somatic motor component of hypothalamus homeostasis

A

Incite appropriate somatic motor behavioral response (directly influence actions)

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7
Q

What is the preoptic area? (POA)

A

Part of hypothalamus critical for temperature regulation

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8
Q

POA

A
  • Thermoreceptive neurons from skin, core, and hypothalamus send info to POA
  • POA integrates temp info and compares to set point
  • POA triggers 3-component response
    ○ Stimulate POA → panting, sweating
    ○ Lesion POA → loss of thermoregulation
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9
Q

POA diagram

A
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10
Q

The POA prioritizes responses to ___

A

Thermoreceptors

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11
Q

What are the most and least important inputs to the POA?

A
  • Most important: hypothalamus temp (can override info from skin & body)
  • Second most important: core body tempt
  • Least important: skin temp (only respond when hypothalamus and core are safe
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12
Q

Somatic response to POA being cooled

A

Seek warmth and shiver

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13
Q

Visceromotor response to POA being cooled

A
  • Increase sympathetic activity (vasoconstriction to prevent loss of heat)
  • Decrease parasympathetic activity
  • Goosebumps (piloerection)
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14
Q

Humoral response to POA being cooled

A
  • Hypothalamus causes release of hormone TSH from anterior pituitary → more release of thyroxine from thyroid gland → global increase in metabolism
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15
Q

Somatic response to POA being heated

A

Seek shade and sweat (panting in other mammals)

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16
Q

Humoral response to POA being heated

A
  • Decreased release of hormone TSH from anterior pituitary → less release of thyroxine in thyroid gland → global decrease in metabolism
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16
Q

Visceromotor response to POA being heated

A
  • Decrease sympathetic activity (vasodilation to shunt blood to periphery & dissipate heat)
  • Increase in parasympathetic activity
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17
Q

Evidence for leptin’s role - ob/ob mice

A
  • Mice lacking both copies of ob gene become obese
  • Ob found to code for protein that tells brain about body’s fat level… leptin
  • An ob/ob mouse given leptin will return to normal body weight
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18
Q

Evidence for leptin’s role – humans

A
  • Some human cases of obesity are caused by leptin and lose body fat when injected with leptin
  • Boy with mutation → produced no leptin → abnormally high weight → synthetic leptin restored normal weight
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19
Q

Ventromedial hypothalamus (periventricular zone)

A
  • Lesion of VM hypothalamus → hyperphagia
    ○ Suggests VM hypothalamus may contain satiety centers
  • Contains the arcuate nucleus
    ○ Has leptin receptors
    ○ Releases peptides that affect appetite
    ○ Critical area for feeding regulation
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20
Q

Lesion of VM hypothalamus leads to ___

A

Hyperphagia

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21
Q

Diagram of effects of lesioning different parts of hypothalamus

A
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22
Q

Where is the arcuate nucleus?

A

VM hypothalamus

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23
Q

Arcuate nucleus

A
  • Has leptin receptors
  • Releases peptides that affect appetite
  • Critical area for feeding regulation
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24
Q

Lateral hypothalamus

A
  • Lesion of L hypothalamus hypophagia, aphagia
    ○ Suggests L hypothalamus may contain hunger centers
  • Lesion of Lateral makes you Little
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25
Q

Lesioning the lateral hypothalamus causes ___

A

Hypophagia, aphagia

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26
Q

Is leptin important for short-term feeding regulation?

A

No, it regulates feeding as body fat changes over time

27
Q

Mad scientist Anna decides to take a naughty mouse and inject a bunch of glutamate into a particular region of the hypothalamus. After the injection, the mouse became insatiably hungry for a while. Where did Adrian inject the glutamate and what’s the term for this outcome?

a) Ventral hypothalamus; hypophagia
b) Lateral hypothalamus; hyperphagia
c) Ventral hypothalamus; hyperphagia
d) Lateral hypothalamus; hypophagia

A

Answer: B - Bonus: What if Adrian lesioned this area?

28
Q

Anorectic peptides (diminish appetite)

A
  • aMSH
  • CART

Don’t eat from the mush cart

29
Q

The ___ releases peptides that affect appetite

A

arcuate nucleus

30
Q

Orexigenic peptides (enhance appetite)

A
  • AgRP
  • M
  • Orexin
  • NPY

Agood Meal Opens Noses

31
Q

Leptin receptors in arcuate neurons

A
  • Leptin stimulates release of anorectic peptides
  • Leptin inhibits release of orexigenic peptides
32
Q

Flow chart of arcuate nucleus response to leptin

A
33
Q

What peptides does leptin cause the arcuate nucleus to release?

A

aMSH and CART

34
Q

Humoral response to leptin & aMSH/CART

A
  • Increased pituitary release of TSH and ACTH
  • TSH and ACTH bind to thyroid and adrenal gland, increasing body metabolism
35
Q

Visceromotor response to leptin & aMSH/CART

A
  • Increased sympathetic ANS activity
  • Increased body temp and metabolism
36
Q

Somatic motor response to leptin & aMSH/CART

A
  • Inhibits MCH & orexin neurons in lateral hypothalamus
  • Inhibited feeding behavior
37
Q

A reduction in leptin causes the arcuate nucleus to release ___

A

NPY & AgRP (orexigenic peptides)

38
Q

Humoral response to less leptin & NPY/AgRP

A
  • Inhibition of pituitary TSH & ACTH release
  • Less TSH and ACTH binds to thyroid & adrenal glands, causing a reduction in body metabolism
39
Q

Visceromotor response to less leptin & NPY/AgRP

A
  • Increased parasympathetic ANS activity
  • Decreased body temp and metabolism
40
Q

Somatic motor response to less leptin & NPY/AgRP

A
  • Stimulates MCH & orexin release from lateral hypothalamus
  • Initiates and promotes eating behavior
41
Q

MC4 receptor in lateral hypothalamus

A
  • The lateral hypothalamus has a receptor called the MC4 receptor that inhibits feeding
  • aMSH activates it → inhibited feeding
  • AgRP inhibits it → stimulates feeding
  • Both peptides competitively bind to this receptor
42
Q

What effect does aMSH have on the MC4 receptor in the lateral hypothalamus?

A

It activates MC4, inhibiting feeding

43
Q

What effect does AgRP have on the MC4 receptor in the lateral hypothalamus?

A

It inhibits it, stimulating feeding

44
Q

The MC4 receptor ___ feeding

A

Inhibits

45
Q

What NTs are suspected to be involved in hunger and satiety regulation?

a) Serotonin
b) Ghrelin
c) Leptin
d) Cholecystokinin
e) All the above
f) Two of the above

A

e) all of the above

46
Q

What factors promote eating in the short term?

A
  • Sight and smell of food
  • Taste and chewing
  • Ghrelin: stomach peptide
47
Q

What factors inhibit eating in the short term?

A
  • Stomach distention that activates that vagus nerve
  • Blood glucose
  • CCK: intestinal peptide
  • GLP-1: intestinal peptide
48
Q

Release of ghrelin

A

Released by stomach cells into bloodstream when stomach is empty

49
Q

Effect of ghrelin

A

Binds to ghrelin receptors, activates NPY/AgRP-containing neurons in arcuate nucleus

50
Q

Evidence for action of ghrelin

A
  • Inject ghrelin → humans eat more
  • Ingest THC → surge in ghrelin levels → munchies
  • Levels increase significantly when dieting
  • Levels decrease rapidly after eating
  • Levels decrease significantly after gastric bypass surgery
51
Q

CCK

A
  • Intestinal peptide released for digestion of fat and protein
  • Binds to CCK receptors in various hypothalamic nuclei, activates aMSH/CART - containing neurons
  • Inject before a meal → reduced appetite (sense of fullness)
52
Q

When is GLP-1 released?

A

After eating

53
Q

GLP-1 effects

A
  • Intestinal peptide released after eating

Satiety effects:
- Slows food going through stomach, prolongs fullness
- Activates vagus nerve (like gastric distension and CCK)
- Binds to GLP-1 receptors in various hypothalamic nuclei, activates aMSH/CART-containing neurons

54
Q

Procedures and treatments involving GLP-1

A
  • GLP-1 Agonists: Semaglutide (Ozempic, Wegovy)
  • Treatment for type 2 diabetes & now obesity
  • GLP-1 levels increase after gastric bypass surgery
55
Q

What are the 2 reasons why we drink water?

A
  • Blood volume is low (hypovolemia)
    → leads to volumetric thirst: seeking water
  • Concentration of ions, proteins, etc. is high (hypertonicity)
    → leads to osmometric thirst: retaining water
56
Q

Renal phase of body’s reaction to loss of volume (volumetric thirst)

A
  • Kidneys detect low blood volume
  • Kidneys secrete renin into bloodstream
  • Renin initiates angiotensin II production
  • Angiotensin II excites neurons in subfornical organ
  • SFO causes magnocellular neurosecretory cells to release ADH into bloodstream
  • ADH causes kidneys to retain water, inhibit urine production
57
Q

Cardiac phase of body’s reaction to loss of volume

A
  • Mechanoreceptors in heart detect decreased blood pressure
  • Send signals up vagus nerve to hypothalamus
  • Hypothalamus activates sympathetic ANS → increased HR, vasoconstriction
  • Hypothalamus also releases ADH → retain water, etc.
58
Q

Hypertonicity → osmometric thirst

A
  • Increase in the concentration of solvents in blood
  • Loss of water by cells is detected by the vascular organ of the lamina terminalis (OVLT)
  • OVLT lacks blood-brain barrier and in telenephalon
  • OVLT neurons exert 2 impacts:
  • Directly excite magnocellular secretory neurons to release ADH
  • Stimulate osmometric thirst (motivation to drink when dehydrated)
  • Can be separately damaged (by OVLT lesion) from systems detecting loss of volume
59
Q

Effects of OVLT neuron activation

A
  • Directly excite magnocellular secretory neurons to release ADH
  • Stimulate osmometric thirst (motivation to drink when dehydrated)
60
Q

Summary of thirst

A
61
Q

A drop in blood volume will lead to a(n)

a) increase in angiotensin II in the blood
b) increase in activity in the parasympathetic nervous system
c) sensors in the major blood vessels signal the vagus nerve and then the nucleus of the solitary tract
d) More than one of the above
e) All of the above

A

d) (B is false because it should be sympathetic nervous system)

62
Q

The lipostatic hypothesis states that

a) the hypothalamus is responsible for the regulation of body weight
b) body fat is maintained homeostatically at a specific level
c) regulation of body weight is based on the relative storage of fat and glycogen

A

b) body fat is maintained homeostatically at a specific level

63
Q

Which of the following molecules is capable of reaching the highest concentration in the blood?

a) CRH
b) ADH
c) oxytocin
d) ACTH

A

d) ACTH

64
Q

Which part of the brain compares the set point with body temp to determine whether heating or cooling is needed?

A

Preoptic area (POA)

A Intro to Neuro (22 decks)

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