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PSYC381 > Final > Flashcards

Final Flashcards

1
Q

what is parental investment?

A

the extent to which parents compromise their ability to produce additional offspring in order to assist current offspring
- species and individuals can adjust their fitness by altering their amount of parental investment into their offspring

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2
Q

what is the optimal strategy for parental investment?

A

each parents provide sufficient care but no more than is absolutely necessary to produce successful offspring

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3
Q

what is the evolutionary trade-off for parental investment?

A

there is an evolutionary trade-off between reproductive effort and parental care, where care for one or few offspring comes at the cost of foregoing the production of more offspring

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4
Q

what are the sex differences in parental behaviour?

A
  • females incur more proximal costs
  • paternal investment is rare
  • paternal investment is generally lower
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5
Q

how do females incur more proximal costs for their investment in offspring?

A

they have to carry + birth the offspring -> choosier sex; males have to compete
- some exceptions (ex. male seahorses lay eggs)

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6
Q

how does paternal investment play a role in sexual selection? what is the difference between low- vs. high-investment males?

A

paternal investment is rare, so sexual selection itself becomes a trade-off between the selection of low- vs. high-investment males
- low-investment males have more time for inter-male competition
- high-investment males are therefore less likely to be able to dominate low-investment males in inter-male competition

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7
Q

why is paternal investment generally lower than maternal investment?

A

males focus their reproductive effect on mating b/c locating and fertilizing as many different females as possible is the best way for males to reach maximal reproductive success; females put reproductive effort into parental care b/c each of its offspring represents a substantial proportion of the female’s life investment of time and resources

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8
Q

how is parental investment a continuum among species?

A
  • vertebrate species provide absolutely no parental care -> female fish lay hundreds of eggs to be fertilized and dips
  • humans provide substantial care and resources for their children for years and decades
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9
Q

what is Hamilton’s rule for altruism?

A

r > C/B, where
- r is the coefficient of relatedness that can range from 0 to 1, such that 0 indicates no relation above average, and 1 indicates a clone
- B is a quantification of the fitness benefit conferred to the offspring
- C is a quantification of the fitness cost incurred by the caregiver

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10
Q

what does Hamilton’s rule for altruism mean?

A

altruistic genes can increase within a population if individuals help close relatives who share copies of the same genes, even at a cost to their own reproduction
- alloparenting is altruistic; investing resources into offspring that has minimal genetic relatedness

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11
Q

how does kin selection promote altruism?

A

can promote alloparenting:
- individuals can increase their overall genetic fitness by helping relatives who share their genes, even if it means sacrificing some of their own resources or chances of survival
- when individuals exhibit altruistic behaviors toward close relatives, they increase the chances that genes shared with those relatives will be passed onto future generations. This creates a selection pressure favoring the evolution of altruism because it indirectly benefits the genes carried by the altruist
- by helping relatives survive and reproduce, even at a cost to oneself, the genes that predispose altruistic behavior can be passed on through shared genetic heritage

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12
Q

what is the parental-offspring theory? how much are parents related to their offspring?

A

depending on the ecological circumstances of a particular species, the time point at which the cost overcomes the benefits varies, but it inevitably arrives
- r=0.5

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13
Q

what are the differences between early- and late-care termination?

A
  • early care termination allows parents to reinvest in new young
  • late care termination allows young to maximize their benefit -> altruistic to put young first rather than maximizing their own reproductive success (I.e. more offspring)
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14
Q

what are altricial and precocial young?

A
  • altricial: being relatively un- or underdeveloped at parturition (ex. humans)
  • precocial: being relatively well developed at parturition (ex. deer born w ability to walk)
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15
Q

what neural structures underlie aggression?

A
  • medial amygdala
  • BNST
  • anterior hypothalamic area
  • PAG
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16
Q

what evidence do fish provide for the implication of prolactin in parental behaviour?

A

midas cichlids feed off the mucus produced in the skin of their parents, which contains prolactin

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17
Q

what evidence do hens provide for the implication of prolactin in parental behaviour?

A

prolactin induces broodiness in hens, allowing females (and often males) to provide parental support by incubating eggs and warming hatchlings
- blood serum from broody hens can induce broodiness in non-broody hens due to prolactin

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18
Q

how does prolactin change in birds over the parental period?

A
  • prolactin levels in mothers remain characteristically high during incubation in essentially all bird species, even for precocial young
  • for altricial young, prolactin levels remain high for the duration of chick-rearing, corresponding to the length of that rearing
  • even parasitic parents (lay eggs in others’ nest) show increases in prolactin immediately after egg laying
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19
Q

what evidence do birds provide for the implication of prolactin in parental behaviour?

A
  • incubation is initiated by high levels of progesterone and sustained by a mid-incubation increase in prolactin
  • crop sacs (where crop milk is produced to feed young) require prolactin, made by both parents
  • in birds, paternal males show increased levels of prolactin similar to females
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20
Q

how do prolactin receptor densities change in birds?

A

prolactin receptor densities increase in the POA during both courtship and brooding

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21
Q

what evidence do humans provide for the implication of prolactin in parental behaviour?

A
  • human mothers rarely show aggressive behaviour to defend their young, but prolactin levels do seem to reflect intrinsic hostility
  • prolactin levels in men show an increase response to the sound of infant crying, but only in men who have childcare experience
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22
Q

what evidence do rats provide for the implication of prolactin in parental behaviour?

A

caecotroph attractiveness is related to maternal prolactin
- caecotroph = nutrient dense product excreted from anus; more prolactin = more pups eating it

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23
Q

what evidence do pregnant rats provide for the implication of prolactin in parental behaviour?

A

pregnant and lactating rats show more brain prolactin receptor activation than virgin rats, including in the following areas:
- telencephalon (septum, BNST, amygdala)
- hypothalamus (POA, PVN, SON, VMN)
- midbrain (periaqueductal gray)

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24
Q

what combination facilitates paternal behaviour?

A

increased prolactin + decreased testosterone

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25
Q

what hormones other than prolactin influence parental behaviour(5)?

A
  • cortisol
  • testosterone
  • estrogen
  • oxytocin
  • progesterone
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26
Q

how does cortisol influence parental behaviour?

A

levels increase in men after the sound of an infant crying, but for both experienced and inexperienced fathers

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27
Q

how does testosterone influence paternal behaviour in humans?

A

levels increase in men after the sound of an infant crying for both experienced and inexperienced fathers, but a more general decrease is proportional to the amount of childcare provided even if they are not the biological father
- less T = more childcare provided

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28
Q

how does testosterone influence parental behaviour in birds?

A
  • nest building in male doves requires testosterone levels to be high
  • testosterone injections in male juncos (birds) decrease paternal behaviour
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29
Q

how does testosterone change over the lifespan in males?

A

fatherhood in humans has the effect of decreasing testosterone beyond the normal observed decrease of being partnered (goes down after marriage; 2 drops)
- decrease most significant during first month after childbirth

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30
Q

how does estrogen influence parental behaviour?

A
  • implants in male MPOAs can induce maternal behaviour
  • in ovariectomized doves, nest building and incubation can be restored by injecting estrogen and progesterone
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31
Q

how does oxytocin influence parental behaviour?

A
  • may decrease levels of maternal aggression, evidence by lesions to the PVN in rat dams
  • oxytocin involved in mother-infant bonding, so decrease OT levels may decrease aggression by decreasing bond (less motivation to defend infant)
  • levels through pregnancy and during labour predict the strength of the mother-child bond
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32
Q

how does progesterone influence parental behaviour?

A
  • incubation is initiated by high levels of progesterone and sustained by a mid-incubation increase in prolactin
  • in ovariectomized doves, nest building and incubation can be restored by injecting estrogen and progesterone
  • in rodents, maternal aggression is correlated with progesterone levels before parturition
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33
Q

what is game theory? what parameters does it contain?

A

the mathematical study of social interactions; contains 4 parameters
- players: the interacting agents
- strategy: the available actions that each player has
- payoffs: the rewards or punishments for their actions
- information: what each player “knows” about the game

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34
Q

how can games be structured?

A

can be simultaneous (moves are made by individuals before other person’s move is known) or sequential (turn-based games), cooperative or noncooperative (working together or competing), discrete or continuous, zero-sum (if I win you have to lose) or non-zero sum

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35
Q

how can emotional states be attributed to strategy for expected payoffs?

A

the evolution and distribution of various emotional states may be attributed to long term strategy for expected payoffs
Ex) jealousy in a relationship: how does it change game strategies? -> motivation to compete, etc.

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36
Q

what is a social dilemma? how does it help us observe social behaviour?what’s an example?

A

when an individual self-interest is pitted against group interest, for groups that the individual belongs to; allows us to observe how people react to such conflict (would one put themself before the group?)
- ex) prisoner’s dilemma

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37
Q

what is the prisoner’s dilemma?

A

2 players can either cooperate or defect against an opponent w/ 4 possible payoffs:
T = temptation to defect (5)
R = cooperation reward (3)
P = mutual punishment (1)
S = sucker’s payoff (0)

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38
Q

what is Pareto efficiency? what is an example?

A

when you can’t improve a move without worsening someone else’s outcome (an alternative move leading to a gain for one player necessitates a loss for the other players)
Ex) gas prices – if one gas station lowers its prices, it takes all customers from other gas stations

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39
Q

what are the 4 social orientations fundamental for any dyad?

A
  • selfishness
  • spite
  • cooperation
  • altruism
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40
Q

what is the evolutionary problem of cooperation and altruism?

A

there is always a temptation to defect due to personal gain, making it difficult for either to become fixed in an evolving population

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41
Q

what are the proposed solutions for the evolutionary problem of cooperation and altruism?

A
  • kin selection
  • direct reciprocity
  • indirect reciprocity
  • network reciprocity
  • group selection
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42
Q

what is kin selection?

A

suggests that altruistic behaviours can evolve if they increase the reproductive success of genetically related individuals (individuals may help their relatives, who share their genes, because by doing so they indirectly promote the transmission of their own genes)

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43
Q

what is direct reciprocity?

A

individuals engage in cooperative behaviours with the expectation that their partners will reciprocate the cooperation in future interactions

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44
Q

what is indirect reciprocity?

A

cooperation is maintained through a system of reputation-based reciprocity, where individuals are more likely to cooperate with others who are known to be cooperative and less likely to cooperate with those known to be uncooperative (paying it forward)

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45
Q

what is network reciprocity?

A

individuals are more likely to cooperate with their direct neighbours in the network, creating clusters of cooperation within the population (individuals are more likely to cooperate if they see cooperation within their network)

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46
Q

what is group selection?

A

individuals in a group benefit from cooperating with each other because groups composed of cooperative individuals are more successful in competition compared to groups with less cooperative members, thus living on in evolution

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47
Q

what is affiliation? what are some associated hormones and evidence?

A

social behaviours that bring animals together
- oxytocin
- vasopressin
- glucocorticoids
- human brain activation

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48
Q

how is testosterone implicated in affiliation?

A
  • in non-territorial manakin males, high testosterone is associated with increased cooperative behaviours
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49
Q

how is oxytocin implicated in affiliation?

A

parental care, grooming, sexuality

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50
Q

what evidence do prairie voles provide for the implication of oxytocin in affiliation?

A
  • monogamous prairie has high levels of OT receptors in prelimbic cortex (emotion), BNST (around amygdala), NAcc (reward), and the lateral amygdala
  • polygamous montane vole shows much fewer OT receptors except in the lateral septum
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51
Q

what evidence do humans provide for the implication of oxytocin in affiliation?

A
  • OT levels are elevated for couples in new relationships (and friendships), and is positively correlated with interactive reciprocity (affective touch, etc.)
  • OT treatment increases males’ partner perception to be more attractive, reflected in NAcc and VTA activity
52
Q

how is vasopressin implicated in affiliation?

A
  • higher V1aR density in ventral pallidum of monogamous prairie voles
  • lower V1aR density in ventral pallidum of polygamous montane voles
53
Q

how are glucocorticoids implicated in affiliation?

A
  • largely drive attachment -> a phenomenon whereby the offspring may experience separation anxiety (different than fear-based anxiety)
  • go up in response to perception of separation
  • corticosterone is related to prairie vole partner preferences in a sex-specific manner
54
Q

how does human brain activation provide evidence for oxytocin and vasopressin implications in affiliation?

A

OT and AVP receptors found in each of these brain regions (modulation):
- images of romantic lovers (compared to friends) activate medial insula and ACC, and deactivate PCC and amygdala
- uniquely romantic activations: hpc, hypothalamus, VTA
- uniquely maternal activations: PAG, OFC

55
Q

what is aggression?

A

social behaviours that drive animals away from each other (threats and attacks)

56
Q

how does testosterone generally facilitate aggression?

A
  • males of most species are more aggressive than females, and testosterone serves to encourage aggression in many species
  • generally, testosterone increases one’s disposition towards risk, and aggressive acts are some of the riskiest behaviours
57
Q

what hormones mediate aggressive bird behaviours throughout the year?

A
  • spring -> antiandrogens and aromatase inhibitors block aggression
  • winter -> neither treatments influence aggression rates
58
Q

how do hormones mediate aggressive behaviours in sparrows?

A
  • castration of males will decrease their levels of aggression in summer, but do not change winter aggression rates
  • aromatase inhibitors will reduce winter aggression -> DHEA plays important role via ARs
  • estradiol seems to rapidly increase aggressive acts in song sparrows only during the nonbreeding period
59
Q

how do hormones mediate aggressive behaviours in red deer?

A
  • castrating male red deer in winter causes them to lose their antlers and sharply decrease in social rank
  • implanting castrated males with T in winter causes them to become more aggressive and regain rank
60
Q

how do hormones mediate aggressive behaviours in siberian hamsters?

A

melatonin increases both DHEA and aggression, mediating the seasonal shift from affiliative to aggressive behaviours

61
Q

how do hormones mediate aggressive behaviours in syrian hamsters?

A

peripubertal exposure to adult aggression will hasten the advent of offensive aggression in the adolescent, increase bullying of smaller opponents, and have slower reduction of attack frequency despite castration

62
Q

what marks the critical organizational period of androgens on adult aggression in mice?

A

postnatal day 6 and puberty

63
Q

how do hormones mediate aggressive behaviours in primates?

A

many are seasonal breeders -> increased levels of T during breeding season correspond to increased levels of male-male aggression (competing for females)

64
Q

how do hormones mediate aggressive behaviours in humans?

A
  • human males show seasonal variation in T but not necessarily correlated with violence, likely because human aggression can be achieved through passive means
  • human girls with CAH show higher levels of rough-and-tumble play (organizational effects of androgens on aggression)
65
Q

what is the challenge hypothesis?

A

integrates data across species to posit that T levels promote social status seeking behaviour -> frequently expressed as aggression, but can also be subtle
- proposed that T promotes aggression when it would be beneficial for reproduction such as mate guarding

66
Q

what is the challenge hypothesis used to explain?

A

used to explain what else testosterone is for besides sperm production

67
Q

what is some evidence for the challenge hypothesis?

A
  • male song sparrow experience T and LH activation after being challenged over territorial dispute
  • 2 peaks of testosterone observed among song sparrows: first during establishment of territory and during the mating period when males guard their sexually receptive mate from other males
  • after fighting between Japanese quail, the winner had elevated T for 3 days after
68
Q

how does oxytocin affect social behaviour in humans?

A
  • OT levels are elevated for couples in new relationships (and friendships), and is positively correlated with interactive reciprocity (affective touch, etc.)
  • OT treatment increases males’ partner perception to be more attractive, reflected in NAcc and VTA activity
69
Q

in what areas of the brain do OT receptors modulate activation?

A
  • images of romantic lovers (compared to friends) activate medial insula, ACC, and CP, and deactivate PCC and amygdala
  • uniquely romantic activations: hpc, hypothalamus, VTA
  • uniquely maternal activations: PAG, OFC
70
Q

how does oxytocin affect aggression and bond?

A
  • may decrease levels of maternal aggression, evidence by lesions to the PVN in rat dams
  • oxytocin involved in mother-infant bonding, so decrease OT levels may decrease aggression by decreasing bond (less motivation to defend infant)
  • levels through pregnancy and during labour predict the strength of the mother-child bond
71
Q

how does oxytocin affect social behaviour in voles?

A
  • monogamous prairie has high levels of OT receptors in prelimbic cortex (emotion), BNST (around amygdala), NAcc (reward), and the lateral amygdala
  • polygamous montane vole shows much fewer OT receptors except in the lateral septum
72
Q

what is osmotic thirst?

A

occurs in response to consuming salty or sugary foods (hypertonic solutions, more solute, blood becomes too salty), increased osmolality in the brain

73
Q

what detects increased osmolality?

A
  • increased osmolality causing osmotic thirst is detected by osmoreceptors: neurons found in the brain in many areas outside the BBB (direct contact w/ CSF)
74
Q

what brain regions have osmoreceptors?

A
  • vascular organ of the lamina terminals (OVLT) -> neurons project to the MPOA which signals the insula (detects changes of sensation of your internal environment) and ACC (motivation + stimulus valuation – water takes priority) to promote drinking
  • subfornical organ
75
Q

what are some properties of osmoreceptors?

A
  • have the protein aquaporin 4 embedded in their membrane to allow water flow
  • membrane stretched inactivated cation channels detect changes in neuron size, signals thirst
76
Q

what needs to be done to quench osmotic thirst?

A

drink water

77
Q

where do osmoreceptors send info to?

A

send information about fluid balance to the PVN and SON (only nuclei that produce ADH, project directly to posterior pituitary), which produce vasopressin

78
Q

what 2 signals does vasopressin send?

A
  • released in mild dehydration (increased distal tube permeability to water, decreasing urine output, facilitating water reabsorption back into blood)
  • stimulate drinking behaviour by stimulating thirst centres
79
Q

what is hypovolemic thirst?

A

occurs in response to the loss of fluid (ex. Blood, loss, diarrhea, etc.); changing amount of fluid you have instead of the concentration of solutes

80
Q

how do you quench hypovolemic thirst?

A

both water and constituent salts must be replaced after acute loss of fluid

81
Q

what detects hypovolemia?

A

cardiac and kidney baroreceptors

82
Q

how do cardiac baroreceptors work?

A

baroreceptors (stretch receptors) in cardiac blood vessels signal ADH release via the vagus nerve, which constricts blood vessels

83
Q

what secretions does hypovolemia cause?

A

hypovolemia (low BP) causes renin production, which converts angiotensinogen to angiotensin I; ANG I is converted to ANG II from angiotensin converting enzyme (ACE) in the lungs

84
Q

what does angiotensin II do?

A

stimulates thirst and the production of aldosterone, which promotes Na+ retention and water conservation in the kidneys; can act as a vasoconstrictor

85
Q

what happens when blood volume is low?

A

hypovolemic thirst detected by cardiac and kidney baroreceptors
- cardiac signals brainstem causing vagus nerve to vasoconstrict vessels
- kidney makes ANG II and acts on receptors in the subfornical organ, vasoconstricting and inducing thirst

86
Q

what happens if solute concentrations are high?

A

osmotic thirst detected by OVLT osmosensory neurons

87
Q

where do both thirst systems project to?

A

preoptic area ->
- hypothalamic thirst network -> stimulates drinking
- supraoptic nucleus, paraventricular nucleus (vasopressin release) -> water conservation

88
Q

what is diabetes insipidus? what is it caused by?

A

causes continuous drinking and urination because ADH is defective

89
Q

what can cause anorexia?

A

bilateral lesions to the lateral hypothalamic area (LHA)

90
Q

what can cause hyperphasia?

A

bilateral lesions to the ventromedial nucleus (VMN)

91
Q

what and where are the 2 hypothalamic circuits that regulate hunger and satiety?

A

arcuate nucleus
- feeding stimulatory circuit: activated during reduced food intake (hungry)
- feeding inhibitory circuit: activated during well-fed state (full)

92
Q

what NTs are produced by the feeding stimulatory circuit?

A

NPY and AgRP; both stimulate food intake
- neuropeptide Y (NPY) signals the PVN to evoke feeding, while Agouti-related protein (AgRP) indirectly promotes feeding by blocking melanocortin type 4 receptors in the PVN (appetite inhibitory receptors)

93
Q

what happens during reduced food intake?

A
  • low fat cell mass causes insulin and leptin concentrations in the blood to be low and have less action in the hypothalamus -> activates NYP/AgRP neurons to produce their NTs and stimulate food intake until leptin and insulins level increase
  • AgRP blocks binding of ⍺-MSH to melanocortin type 4 receptors, decreasing its activity and increasing food intake
  • low insulin/leptin simultaneously inhibits POMC/CART neurons in the arcuate nuclei, reducing ⍺-MSH (inhibits food intake)
94
Q

what 2 main signalling molecules are produced by the feeding inhibitory circuit?

A

cocaine and amphetamine-related transcript (CART) and pro-opiomelanocortin (POMC)
- increased CART secretion in the PVN decreases food intake
- POMC produces ⍺-MSH which acts on melanocortin type 4 receptors to inhibit appetite

95
Q

what happens during the well-fed state?

A
  • high fat cell mass causes leptin and insulin concentrations in the blood to be high and have more action in the hypothalamus -> activates POMC/CART neurons to secrete their products into the PVN and LHA
  • causes increased ⍺-MSH expression and release into the PVN and activates more melanocortin receptors, decreasing food intake
  • high insulin/leptin simultaneously inhibits NPY/AgRP neurons, decreasing their NT expression and reducing AgRP inhibition of melanocortin receptors, ultimately reducing food intake
96
Q

what are the 2 satiety signals of the hindbrain?

A
  • mechano (stretch of stomach and liver detected by vagus nerve and projects to the NTS)
  • hormonal (leptin and insulin act on arcuate nucleus)
97
Q

what is the stress response?

A

set of physiological and behavioural responses that help to reestablish homeostasis

98
Q

what 2 endocrine systems constitute the major components of the stress response?

A
  • epinephrine from adrenal medulla (due to SNS activation, occurs first)
  • glucocorticoids from adrenal cortex (occurs after SNS response)
99
Q

what happens when there is a perceived threat?

A
  • within hundreds of msecs the amygdala stimulates the hypothalamus and sympathetic nervous system towards a state of heightened arousal, or if the stressor is perceived to be a strong enough threat: the fight-or-flight response
  • within seconds the adrenal medulla releases epinephrine and the HPA axis stimulates the release of cortisol
100
Q

what does epinephrine mediate?

A

fight-or-flight response: changes in cardiovascular tone, respiration rate, blood flow to muscles; E (and NE) help mediate these changes + increase glucose levels to fuel this response

101
Q

how does activation of the HPA axis lead to glucocorticoid release?

A

stressor causes corticotropin releasing hormone (CRH) to be secreted from the hypothalamus (PVN), which signals the anterior pituitary to secrete adrenocorticotropic hormone (ACTH) -> released into the bloodstream to signal adrenal cortex to secrete corticosteroids

102
Q

what receptors do glucocorticoids act on?

A
  • mineralocorticoid receptors (MRs)
  • glucocorticoid receptors (GRs)
103
Q

what receptors does CRH act on?

A

CRH1 and CRH2 receptors

104
Q

how can GRs stimulate the relreae of endocannabinoids?

A
  • corticosterone binds GR (GPCR) on postsynaptic neuron, activates Gs, increased cAMP activates PKA, synthesizes endocannabinoid (eCB)
  • eCB acts on GABAergic CB1 receptor to inhibit GABA release, enhancing NE releases (removing its inhibition)
105
Q

what happens to offspring of chronically stressed mothers (dams)?

A

altered brain morphology, physiology, and behaviour
ex) lower prolactin

106
Q

what are the psychophysiological effects of exposure to high levels of stress prenatally in humans?

A

maternal cortisol may dysregulate the stress response and lead to health consequences
- increased amygdala size in girls, reduced birth weights, developmental delays, attentional deficits, hyperanxiety, etc.
- elevated cortisol levels during pregnancy associated with poor emotional development in girls (due to increased right amygdala activation)

107
Q

what are the psychophysiological effects of exposure to high levels of stress neonatally?

A
  • experience with mild stress early in life is associated with increased coping ability later in life, but chronic stress causes dysregulation
  • in rats, female pups are more sensitive to the effects of prolonged stress than male pups
108
Q

how can early stressors organize the brain to be more effective at coping with stress later on in life?

A

GR expression increases in pups in response to maternal behaviours, increasing stress sensitivity buffer
- epigenetic demethylation of the GR gene and acetylation of histones around GR increase its expression
- high pup stress predicts stressful life

109
Q

what do receptor antagonists tell us about NE’s role in learning and memory?

A
  • phenoxybenzamine is an ⍺ receptor antagonist -> dose-dependent memory enhancement
  • propranolol is a β receptor antagonist -> dose-dependent memory impairment
110
Q

how can peripheral NE interact with central NE?

A

β-receptors on peripheral nerves can integrate hormonal signals with central NE via the nucleus of the solitary tract (NTS) (vagal complex)
- projects to basolateral amygdala -> modulates/enhances memory of emotional experiences

111
Q

how else can NE affect learning and memory?

A
  • inverted-U shape between arousal (NE) and memory performance
  • heightens alertness and attention which can facilitate learning
112
Q

how can cortisol improve memory?

A
  • acute stress and release of cortisol improves the consolidation of memory
  • cortisol facilitates hippocampus-dependent processes (ex. trace conditioning)
113
Q

how does chronic stress affect memory?

A

chronic stress and high levels of cortisol act as amnestics (disrupt memory), through dysregulation of the HPA axis, and desensitized amygdala and hippocampus

114
Q

how is the effect of cortisol on memory similar to NE?

A

cortisol has similar inverted-U shaped effects on memory as NE, in both dose-dependent and temporal patterns of exposure

115
Q

what do GR agonists and antagonists tell us about learning?

A

GR agonists like dexamethasone facilitates passive avoidance learning, while GR antagonists impair learning effects

116
Q

how does high cortisol affect the hippocampus?

A

hippocampus has dense GR expression; high acute or chronic dose has the effect of decreasing:
- number of pyramidal cells
- dendrite lengths
- number of dendritic branch points in CA1 and CA3

117
Q

how is hippocampal neurogenesis affected by cortisol?

A

hpc neurogenesis rate is responsive to levels of cortisol (stress inhibits neurogenesis)
- Cushing’s disease: high cortisol reduces volume
- Addison disease: low levels of cortisol reduces granule cell number, impairs memory

118
Q

how do low levels of cortisol affect the hpc?

A

decreases the size of the dentate gyrus

119
Q

what are some of the distinguishing endocrine correlates for major depressive disorder?

A
  • thyroid hormones
  • prolactin
  • cortisol
  • estrogens
120
Q

how are thyroid hormones related to MDD?

A
  • depressed people tend to have low thyroid function, have a smaller than normal thyroid-stimulating hormone (TSH) elevation in response to thyrotropin-releasing hormone (TRH) stimulation; TRH treatment can reduce depression
  • depressed patients exhibit high levels of antibodies against thyroid gland, high TRH concentrations in CSF, and enhancement of antidepressant efficacy when cotreated with T3
121
Q

how is prolactin related to MDD?

A

elevated blood plasma levels of prolactin in depressed patients

122
Q

what levels of cortisol are associated with depression?

A

can result from either high or low cortisol
- Cushing syndrome: cortisol overproduction
- Addison disease: cortisol underproduction

123
Q

what is a predictor for future depression?

A

chronic anxiety is often a predictor of future depression – blunted negative feedback response to cortisol is a symptom

124
Q

what do cortisol levels look like throughout the day in people with depression?

A

both baseline cortisol levels and peak morning surge are higher for most people suffering from major depression, and are also highest ~3-4 hours after sleep starts

125
Q

how else is cortisol implicated in MDD?

A
  • dexamethasone typically dampens cortisol secretion; fails to sustain suppression in depressed patients
  • high CRH in CSF
  • normalization of cortisol levels through treatment often leads to a resolution of depression symptoms
126
Q

how are estrogens implicated in MDD?

A
  • low levels of estrogen generally decrease mood, and there is a strong relationship between menstrual phase and these symptoms
  • in a double-blind study of depressed women, ~90% given estrogens improved and ~half of controls worsened
  • estrogen improves mood in postmenopausal women, and depression resumes once estrogen treatment ceases

PSYC381 (2 decks)

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