Chapter 9: Homeostasis, Motivation & Reward Flashcards

exam 3 material

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1
Q

what is homeostasis?

A

steady internal balance or equilibrium, regulatory systems actively defend certain values or set points

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2
Q

what part of the brain is essential to homeostasis?

A

the hypothalamus

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3
Q

what kind of mechanisms regulate body temperature?

A

a precisely defined set point, mechanisms that can detect deviations away from the set point, internal and behavioral elements designed to regain the set point

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4
Q

what are the two solutions for maintaining internal temperature in animals?

A

endotherms: internal metabolic activity
ectotherms: external factors, such as sunlight or warm surfaces

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5
Q

what are the autonomic internal responses to low or high body temperature?

A

low: shivering, blood vessels contract, thyroid hormones increase to boost metabolic rate
high: perspiration, licking, panting, blood vessels dilate near skin surface

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6
Q

what part of the brain is responds to higher temperatures?

A

preoptic area (POA) of the hypothalamus has warm-sensitive neurons
POA -> paraventricular nucleus (PVN) -> lateral hypothalamus (LH) -> parasympathetic activity = cool down

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7
Q

what part of the brain is responds to lower temperatures?

A

posterior hypothalamus has cold-sensitive neurons, receive inhibitory input from the warm-sensitive neurons
POA -> PVN -> sympathetic activity = conserve/generate heat

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8
Q

what are the body fluids made up of?

A

electrolytes: sodium, calcium, potassium, chloride, and magnesium

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9
Q

what are the three major fluid compartments in our body?

A
  1. extracellular fluid: higher concentrations of Na and Cl (blood supply and CSF)
  2. intracellular fluid: higher concentrations of K
  3. interstitial fluid
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10
Q

what are the mechanisms of osmotic thirst?

A

drop in the intracellular fluid volume detected by osmoreceptors located in the organum vasculosum of the lamina terminalis (OVLT)

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11
Q

what are the mechanisms of hypovolemic thirst?

A

drop in blood volume, baroreceptors in heart and kidneys measure blood pressure

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12
Q

how does the body respond to thirst?

A

osmoreceptors and baroreceptors stimulate release of vasopressin from the posterior pituitary gland, this stimulates our kidneys to reduce urine productions and constrict blood vessels

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13
Q

how does the body initiate drinking?

A

angiotensin II acts on subfornical organ (SFO), the SFO then communicates with the medial POA which receives input from the nucleus of the solitary tract (NST), the NST receives input from baroreceptors and osmoreceptors and the zona incerta stimulates drinking to the motor system

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14
Q

what are some important neurochemicals involved in hunger?

A

insulin, glycogen, glucagon, leptin, ghrelin, NPY, POMC, and orexins

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15
Q

what does digestion do?

A

breaks down foods into usable chemicals by the digestive tract, excess glucose is stored as glycogen in the liver and excess fat is stored in adipose tissue

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16
Q

how do glucagon and insulin regulate glucose levels?

A

glucagon converts stored glycogen back into glucose
insulin helps store glucose as glycogen (assists in moving glucose from the blood supply into cells)

17
Q

type 1 vs type 2 diabetes

A

type 1: disorder of insulin production, diagnosed in childhood or early adulthood
type 2: disorder of insulin recognition by cells, adult onset, obesity is a major risk factor

18
Q

what are the hunger and satiety neural circuits?

A
  • PVN, LH, arcuate nucleus, VMH
  • VMH lesions produce hyperphagia
  • LH lesions inhibit eating (homeostatic set-point changes)
  • hunger activates the vagus nerve and raphe nuclei -> PVN and LH
  • hormones in the arcuate nucleus -> LH, VMH, PVN
  • PVN -> arcuate nucleus, VMH, LH
19
Q

how do leptin/insulin, NPY/AGRP, and ghrelin influence eating behavior?

A

leptin and insulin communicate with the arcuate nucleus when glucose levels are low
NPY/AGRP activation stimulates feeding via PVN -> PNS activation, high leptin inhibits hunger via POMC
ghrelin increases when hungry and stimulates feeding

20
Q

what role does orexin play in hunger?

A

orexins are produced in the LH, neurons that release orexins project widely in the cerebral cortex, midbrain, and pons, injection of orexins into the LH results in increased eating in rats, leptin, glucose, and ghrelin levels appear to regulate orexin signaling, orexin activates NPY

21
Q

what is the medial forebrain bundle brain reward pathway?

A

contains both ascending and descending fibers that pass through the lateral hypothalamus, connecting with the ventral tegmental area (VTA)

22
Q

what is the mesostriatal brain reward pathway?

A

innervated with dopamine neurons, most addictive substances act as dopamine agonists, especially in the nucleus accumbens

23
Q

how was the reward circuit discovered?

A

Olds and Milner study which found that rats would press a lever in order to receive a small joint of current in the LH, indicating that there are reward mechanisms in the brain involved in positive reinforcement

24
Q

what neurotransmitters contribute to reward?

A

dopamine contributes to reward-seeking and learning, essential to “wanting” but not necessarily “liking”, serotonin, glutamate, and GABA signaling are also important in processing reward and promoting goal-directed behavior

25
Q

wanting vs liking

A

wanting is characterized by more motivational factors such as desire and craving (dopamine is key to wanting), liking describes pleasure and hedonic responses to a reward, such as our enjoyment of foods (opioid and endocanabinoid systems are key in liking)

26
Q

how does SUD alter the brain?

A

becoming intoxicated activates the reward circuits in the VTA and basal ganglia (mediated by dopamine and endorphins), withdrawal is associated with increased amygdala activity (increased CRF and dynorphin activity), withdrawal leads to preoccupation (mediated by PFC deficits)

27
Q

how does SUD alter homeostasis?

A

chronic drug use causes dopamine responses to become blunted and body struggles to maintain homeostasis, stress symptoms become overactive during drug withdrawal

28
Q

how does SUD alter impulsivity?

A

chronic drug use blunts activity in the frontal cortex, reduced volume of the OFC is associated with impulse behavior

29
Q

what role does orexins play in SUD?

A

orexins are stimulated by morphine conditioned place preference (CPP), stimulating orexins reinstates morphine seeking behavior in rats

30
Q

how is food addiction similar and different to addiction?

A

same: increased activity in salience and reward networks, reduced activity in executive control networks
differences: drugs work directly on the brain, not all individuals with obesity can be diagnosed with a food addiction