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Psy 106 > EXAM 3 > Flashcards

EXAM 3 Flashcards

1
Q

idea that sensory feedback from our facial expressions can affect our mood

A

facial feedback hypothesis

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2
Q

process in which animals will work to provide electrical stimulation to particular brain sites, presumably bc the experience is rewarding

A

brain self-stimulation

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3
Q

collection of axons traveling in midline region of forebrain

A

medial forebrain bundle

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4
Q

region of forebrain that receives dopaminergic innervation from the ventral tegmental area, often associated with reward and pleasurable sensations

A

nucleus accumbens (NAc)

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5
Q

sudden intense emotion characterize by actions, such as snarling and biting in dogs, that lack clear direction

A

decorticate rage

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6
Q

loosely defined, widespread group of brain nuclei implicated in emotions that innervate each other to form a network

A

limbic system

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7
Q

region of cortex lying below the surface, within lateral sulcus, of the frontal, temporal, and parietal lobes

A

insula

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8
Q

composed of several psychological constructs, rooted in biology
arouses an organism toward desired goal which is the reason for action

A

motivation

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9
Q

examples of motivated behaviors

A

eating/drinking, sex/reproduction, sleep activity, curiosity/exploration, socializing, taking drugs, gambling, risk taking

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10
Q

core hedonic pleasure, rewarding-seeking behavior
composed of conscious pleasure and core hedonic (subcortical/ w/conscious awareness) pleasure

A

liking

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11
Q

motivation for reward, reward seeking behavior. Natural rewards elevate dopamine levels. Composed of conscious desires and incentive salience

A

wanting

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12
Q
  • claims liking and wanting conscious mechanisms that likely involve cortical structure
  • also have subcortical circuits, homologous with animals, below level of perceptual awareness
  • believes that wanting and liking can be influenced by learning–associations, representations, and predictions about future rewards based on past experiences
  • demonstrated that these psychological components are mediated by dissociable brain substrates
A

Berridge

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13
Q

“liking regions”

A

nucleus accumbens and ventral pallidum

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14
Q

“wanting regions”

A

ventral tegmentum
amygdala
ventral pallidum
nucleus accumbens
prefrontal and insular cortex -> incentive saliences processing

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15
Q

deep in brain-> nucleus accumbens, ventral pallidum, brainstem
-other candidates in cortex -> orbitofrontal, cingulate, medial prefrontal and insular cortices
-cortical regions involved in conscious awareness of pleasure/liking

A

hedonic pleasure mechanism location

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16
Q

dopamine pathways

A

1) mesolimbic
2) mesocortical
3)nigrostriatal
4)tuberhypophyseal

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17
Q

dopamine pathway with cell bodies in ventral tegmental area (VTA) and axons in nucleus accumbens

A

mesolimbic pathway

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18
Q

dopamine pathway with cell bodies in VTA and axons in prefrontal cortex, ventromedial prefrontal cortex

A

mesocortical pathway

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19
Q

dopamine pathway with cell bodies in substantial nigra and axons in striatum

A

nigrostriatal pathway

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20
Q

dopamine pathway within hypothalmus

A

tuberhypophyseal pathway

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21
Q

placed into these brain regions increases conscious subjective pleasure

A

conscious pleasure: OPIATES

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22
Q

orbital frontal cortex, anterior cingulate cortex, insular cortex/insula

A

conscious pleasure: CORTEX REGIONS

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23
Q

placed into these brain regions, increases subcortical subjective pleasure

A

core hedonic pleasure: OPIATES

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24
Q

NAc shell, ventral pallidum, periaqueductal gray (AG), amygdala

A

core hedonic pleasure: REGIONS

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25
Q

natural rewards

A

microdialysis

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26
Q

-less actions in female development
-default is female
-dont need estrogen secretion; natural process while testes must be turned on the other hand must be turned on in 2nd month of development
-estrogen needed for brain growth

A

development of sexual differentiation of females as indirect genetic effect

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27
Q

undifferentiated gonad -> chromosomal sex (XX vs XY) -> gonadal sex (ovaries vs. testes) -> sexual phenotype (vagina or penis)

A

normal sex differentiation (classic/simplistic model)

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28
Q

1)males inherit X and all its genes from Mom so any genes one X important for development in brain function come from mom
2) females have 2X-one is randomly expressing most cells
3)some cells express double dose of X

A

direct genetic effects in sexual dimorphism

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29
Q

XY
important b/c males have only 1 X and its from mom
-> sex-linked disorder prominent due to one faulty X

A

male chromosomes

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30
Q

XX
-one X is inactivated in most cells (Barr body)
-some cells use double dose of X
-some cells-X from mom, others- X from dad (random distribution
ex-phenomenon in calico cats mosaic-like patches
–all are female-> coats show X inactivation

A

female chromosomes

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31
Q

evidence that activational actions of hormones alone can change regions
-region of amygdala, the MePD, increases and decreases in size dependent on testosterone levels in males and females
-> we see change in amygdala in human males when they approach and pass puberty when testes turn on and start secreting testosterone
-> also true that unless male mice get chance to show rough-and-tumble play as juveniles, their MePD does not get large, remaining small like females

A

activational action of hormones and brain regions

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32
Q

1)regions of hypothalamus-LeVay studies
2)corpus callosum-different shape in female, may be related to differences in asymmetry between hemispheres of males and females (ex-males more lateralized in language)
3) differences in use of brain regions-> for some tasks, females use both hemisphere while men use only one
4) differences in structure and function of the amygdala-emotion regulation may be different in males vs. females
5)disproportionate representation of certain neuropsychiatric diseases between sexes
6)sex differences in regions of brain involved in reward
-both liking and wanting areas
-mPOA sends axons to VTA which then activate NAc and accessory olfactory bulb (AOB)

A

sexually dimorphic brain regions in humans

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33
Q

individuals have minimal 5-alpha reduces to convert testosterone to dihydrotestosterone
-while internal testes and duct system are male , external genitals which require dihydrotestosterone for development are feminine at birth
-@ puberty, when hypothalamus and pituitary secrete large quantities of GNRH, LH, FSH, the testes up regulates 5 alpha reductase activity and more dihydrotestosterone is produced
-> genitals grow and become masculine at puberty
-some remain female, but most live rest of lives as male
**When it was initially thought that these individuals proved that gender identity was fluid and could easily be altered, later research showed that these individuals were not raised as girls but as 3rd sex
–recognized as different and expected to become male at puberty
–thus, it is hard to disentangle environment and hormones from syndrome

A

Guevadoces / 5-alpha reductase deficiency

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34
Q

-these individuals have no androgen (testosterone) receptors and therefore cannot react to high levels of androgen their testes secrete
-born with female phenotype except for testes that do not descend due to lack of scrotum
–internal and external phenotype is otherwise female
-> v female behaviors and preferences with no evidence of masculinized behavior
**suggests that gender identity, sexual pref, and gender-related behaviors are not directly influenced by presence of Y chromosome

A

Androgen-Sensitivity Syndrome

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35
Q

-genetic abnormality in which an enzyme is missing from adrenal gland of fetus
–causes adrenal to fail to produce sufficient cortisol such that no negative feedback to hypothalamus (CRF) or pituitary (ACTH) occurs
-thus, lots of CRGF and ACTH are released and the adrenal is stimulated to produce excess androgens, including testosterone and dihydrotestosterone
-resulting levels are between normal male and female (intermediate)
-usually, individual born with masculinized genitals so often raised male due to masculine phenotype at birth
-others have feminizing genital surgery
–these individuals display more rough-and-tumble play, prefer male-type toys, and more typical behavior/pref than matched female relatives. Also are more likely to report homosexual fantasies. BUT have clear female identity
**data suggest that gender-related behaviors are influenced prenatally by high androgen levels and that sexual preference may also be influenced to some degree
-HOWEVER, gender IDENTITY may not be as readily influenced

A

adrenogenital syndrome

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36
Q

-BKGD: one twin’s penis was severely burnt at 8mo and was raised as girl until age 14. Underwent surgery and hormone therapy to live life as man, post-revelation of accident
**clinical case suggests that gender identity, sexual preferences, and gender-related behaviors are not easily reversed by environmental factors, at least after 1 year of age
-> boy raised as girl showed lots of rough-and-tumble play and did not like to do “what girls like to do”

A

Clinical Case of Twin Boys, One Raised as Girl

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37
Q

discovered a sexually dimorphic nuclei in hypothalamus of human brains
-in cluster of 4 regions of hypothalamus (INTERSTITIAL NUCLEI), 2 are sexually dimorphic, but not homologous with SDN of rats
-interestingly, in autopsy data of heterosexual men, homosexual men, and females, one of interstitial nuclei in homosexual men is small, like that of females
**Finding does NOT tell us anything about genes, hormones, or experiences leading to morphological difference in human brain that appear to be associated with male homosexuality (early or lack of hormone exposure? differential hormone exposure? AIDS exposure (autopsy!)? behavioral differences?)

A

LeVay

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38
Q

found a sexually dimorphic nucleus in spinal cord that functions to control penile movement in rat
-turns out testosterone (not estradiol) is needed for male-like region to develop
-female rats given testosterone at birth have large regions in their spinal cord that control penile movement, even though they don’t have a penis
**brain sexual dimorphism can develop independent of functional output

A

Breedlove

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39
Q

showed that nuclei in songbird brain that control song are highly sexually dimorphic, just like behavior.
-females have tiny or nonexistent regions compared to large, well-developed regions in males

A

Nottebohm

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40
Q

sexually dimorphic nucleus of preoptic area is 3-5x larger in males than females due to testosterone
-giving female testosterone promotes axon growth but estradiol does not
-testosterone is converted to estradiol in female ovaries

A

R. Gorski study

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41
Q

1)Y -> SRY gene -> stimulates Sox9 gene on Chromosome 17
2)SRY gene expression leads to teste formation, which produces Leydig and Sertoli cells
3)Leydig cells produce testosterone, which leads to internal Wolffian duct system
-5-alpha reductase coverts testosterone to dihydrotestosterone, which leads to external male genitals
4)Sertoli cells produce Anti-Müllerian hormone, leading to the regression of female Müllerian duct system (disappearance of ovaries and Fallopian tubes)
-androgen receptors on X chromosome

A

development of sexual differentiation of males as indirect genetic effect

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42
Q

-males and females have different levels of androgens,estrogens, and somewhat different brain circuitry
-> if you give an adult female rat testosterone, it wouldn’t desire sex with other females (and vice versa with males and estrogen)
-clear sex differences in male and female brains, likely related to circuitry
-> sex differences in many neuro and psychiatric disorders (ex-females: Alzheimers, anxiety, depression, MS, anorexia. males: dyslexia, autism, Tourette’s)

A

Sexual dimorphism of brain composition

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43
Q

-conserved node
-sexually dimorphic
-social, sensory input
-stimulation from VTA and AOB
-widespread connections
-molecularly heterogenous
-periphery signals

A

dissection of medial preoptic area (mPOA) circuit

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44
Q

-in females, circulation of hormone leads to arousal behavior, such as Lordosis response (arched back)
-receptive field of skin and flank become very sensitive
-affects neurons at periaqueductal grey, ventromedial hypothalamus, medullary reticular formation, reticulospinal tract, spinal cord
-medulla acts as way station

A

estrogen

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45
Q

activation hormone most dominant in males
-kind of androgen
-more testosterone (above normal) does NOT increase sex drive in rats BUT removing source of testosterone (testes) via castration decreases sex drive
-sensory and motor system sensitivity

-converted to estrogen and act on mPOA and medial amygdala
- act on spinal neurons to augment reflex
-act on muscles, including erectile muscles
-receptors in ventral midbrain, acting as way station
-receptors in olfactory bulb vital for smell and for vomeronasal system

A

testosterone

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46
Q

long lasting effect of hormones (or other chemical) that alters that trajectory of development
-usually during early development
-influence synaptogenesis and cell death
-affect circuitry => long lasting

A

organizational effects of hormones

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47
Q

-short acting effect of hormones, drug, or other chemicals, usually at puberty and beyond
-like light switch
-hormones prime brain to modify processing of social info, such as opposite-sex mate cues and infant cues
-leads to development and turning on of behavior, return of reactivity to stimuli

A

activational action of hormones

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48
Q

-direct-encouraging sports in boys but not girls
-indirect-“mothering” may have different effect on biological males and females

A

early experiences as cause of sex differences and sexually dimorphic behaviors

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49
Q

-different hormones-male have lots of testosterone, females have lots of estradiol
-having circulating hormone or not-activational actions
-exposure to testosterone and hormones early in human development (end of 1st trimester)

A

hormone differences as cause of sex differences and sexually dimorphic behaviors

50
Q

direct-direct gene action
indirect-genes make gonads, gonads produce hormones

A

genetic differences as cause of sex differences and sexually dimorphic behaviors

51
Q

1) genetic differences (Direct and indirect)
2) hormonal differences
3)early experiences
=not innate differences in sense of “immutable”-brain difference does not directly reveal how change happened

-different brain regions become different in males and females via different mechanisms (activational hormones, organizational hormones, experience, direct genetic effects, or some combination).
–therefore, it is possible that one brain region could be more “male-like” or “female-like” than other regions
–each brain its likely a mosaic of more or less male-like or female-like structures and functions

A

causes of sex differences and sexually dimorphic behaviors

52
Q

biological differences between males and females, in organs, hormones, and body shape
-different expression of similar behaviors in males and females
ex) male rats mount females during sex. females show perceptivity and receptivity
-female rats and humans acquire self-administration/addiction to cocaine more rapidly and at lower doses than males. females do it more in response to stress while men do it more in response to drug cues

A

sex differences

53
Q

Complete differences in physical characteristics between males and females of the same species.
ex) male zebrafinches sing to attract females. females lack neural circuitry to sing

A

sexual dimorphism

54
Q

prevent pair bonding

A

dopamine agonists in courtship/mating

55
Q

-arginine-vasopressin (AVP) and oxytocin (OT) are released in sexual behavior and these hormones appear to be involved in social bonding
-data from studies suggest that it might be the difference in AVP receptor binding in these reward areas that might make prairie voles rewarded by social attachment, while meadow voles don’t have receptors in right location, explaining why they aren’t reward by partner cuddling

-Larry Young et al tested this hypothesis w/ virus to induce AVP expression in meadow voles in ventral palladium where prairie voles had receptors
-data shows that when you increase expression of AVP receptors in ventral palladium of meadow voles, they then show social bonding/cuddling with female after mating like prairie voles

-other work has shown that if you use a drug to. block AVP receptors in these now “prairie-vole-like” meadow voles , then they return to acting like meadow voles (no interest in females post sex)
-also, species difference in distribution of oxytocin receptors between monogamous and polyamorous voles
-in NAc, caudate putamen in BG, and prefrontal cortex in monogamous voles but not polygamous
-oxytocin release in NAc normally stimulates partner preference

A

Prairie Voles (monogamous) and Meadow Voles (polygamous)

56
Q

1) manipulate hormone and see effects on behavior
ex-take away hormone or administer exogenously
-somatic approach
2)manipulate behavior and see effect on hormone secretion
ex-give male access to female
-behavioral approach
3)determine natural variation in hormones and relate them to changes in behavior of animal
-correlation
4)determine how environmental events modify components of hormone sensitive behavior or alter brain?
ex-time of day, season of year, stress, social interactions
-somatic approach

A

strategies used to determine steroid hormone modulation of sexual behavior

57
Q

preoptic area (POA) - fewer receptors in females than males but not a different general location
-but both sexes have androgen and estradiol receptors in brain

A

sex based differences in androgen receptors

58
Q

-exert their effect in indirect fashion
-when hormones reach target organ/tissue, they can be easily absorbed into cells bc cell membranes are made of fat
-inside of some cells are protein receptors, specific to these hormones, in cytoplasm
-when steroid hormones bind to receptor protein, change in protein’s native conformation converts inactive receptor to active DNA-binding state, thereby enabling protein to chemically interact with cell DNA
–once steroid hormone has attached itself to receptor, pair goes into nucleus of cell and interacts with DNA, thereby controlling transcription of other genes
=> result is change in protein synthesis and is process that can take min/hr/days
–steroids hormones working in this classic fashion tend not to exert effects as quickly but can have rapid effects in membrane bound receptors
-androgen and estradiol receptors are not randomly distributed but are cluster in a region of midbrain, many regions of hypothalamus, basal forebrain, and lightly in hippocampus and neocortex

A

estradiol and testosterone

59
Q

made in neurosecretory cells in hypothalamus
-neurons extend their axons into posterior pituitary (part of brain) and these peptide hormones are released each time the neurons fire

-works peripherally in body and centrally in brain
-increases uterine contractions during birth and milk letdown during suckling, social bonding/affiliation

-experiments supporting view that this hormone facilitates social bonding in species that have receptors for these hormones in their reward pathways
-social bonding/mate preference appears to only occur when these receptors are in NAc
-enhance dopamine release in NAc, enhancing reward value of mate(“wanting”)

A

oxytocin

60
Q

made in neurosecretory cells in hypothalamus
-neurons extend their axons into posterior pituitary (part of brain) and these peptide hormones are released each time the neurons fire

-acts via metabotropic receptor and has both peripheral actions on body and central brain actions
-increases resistance of blood vessels and through this action, increases BP, regulating H2O balance, memory, and social bonding

-experiments supporting view that this hormone facilitates social bonding in species that have receptors for these hormones in their reward pathways
-social bonding/mate preference appears to occur only when these receptors are in ventral pallidum
-enhance dopamine release in NAc, enhancing reward value of mate(“wanting”)

A

vasopressin

61
Q

endocrine gland that is not part of brain
-stimulated by LHRH and FSRH to release FSH and LH to stimulate gonads

A

anterior pituitary

62
Q

hormones secreted by the adrenal cortex
-estrogens, androgens, glucocorticoids
-may have some membrane bound receptors but are mostly in cytoplasm
*testosterone, estradiol, and progestins are secreted from gonads but their secretion is controlled by hypothalamus via secretion of leutinizing hormone releasing hormones or follicle stimulation hormones (LHRH/FSRH)that stimulate anterior pituitary to release FSH/LH, which stimulate gonads

A

steroid hormones

63
Q

-big different is distance travelled
*NT=locally released and attach to receptor v. nearby
*hormone=can be released in body and travel in blood to neurons in brain (less fast acting than NT)

-some hormones attach to receptors in cytoplasm and not just membrane bound receptors
*steroid hormones
*other hormones are peptides/proteins, large molecules that once released into blood can’t return to brain, but bind like NT (ex-vasopressin and oxytocin)

A

differences between NT and hormones

64
Q

both are chemical messengers that attach in lock and key fashion to specific receptors

A

similarities between hormones and NTs

65
Q

glands that secrete chemicals called hormones directly into the bloodstream

A

endocrine glands

66
Q

chemical messengers that are manufactured by the endocrine glands, travel through the bloodstream, and affect other tissues
-exert chemical control over some processes that are occurring in that location
-can be made in brain itself and released more locally (neurons have some hormone receptors)
-receptors not in all cells-> location of cells with receptors determines what the target of the hormone is

A

hormones

67
Q

-highly polymorphic and conserved set of genes that plays an important role in immune function of vertebrates
-both mice and humans have been shown to prefer body odor of potential partners that have dissimilar MHC
–complimentary MHC may confer added immune resistance to offspring, making them less susceptible to disease
-> studies have shown that human females with low, steady estradiol from OC use prefer males with similar MHC (maladaptive)

A

Major Histocompatibility Complex (MHC)

68
Q

the sexually arousing power of a new partner (greater than the appeal of a familiar partner)
-sexual motivation and preference increased by novelty
-studies have shown that animals from polygamous species choose partner that present different sensory cues than their most recent partner

A

Coolidge effect

69
Q

-3rd component of reproductive behavior
-motor control and hormonal modulation of sensory-motor pathways

A

mating

70
Q

-2nd component of reproductive behavior
-requires hormonal modulation and “wanting” system

A

courtship/social affiliation/bonding

71
Q

-first component of reproductive behavior
-includes partner preferences
-involves perceptual systems, such as vision, smell/taste, touch, hearing, and “liking systems”
–respond best to change/novelty
-evidence for smell influence- MHC
-evidence for auditory influence-preference for zebra finches with more songs elements (potential link to increased intelligence)

A

attraction

72
Q

-all have different neurochemical/neurohormonal controls and pathways
1)attraction
2)courtship/social affiliation/bonding
3)mating

A

3 components of reproductive behavior

73
Q

-building off how oxytocin increases when rats are in contact
-shows that oxytocin receptor levels in hypothalamus increases following stress
–data suggest (but don’t prove) that stress may make rats more sensitive (more receptor) for oxytocin and oxytocin may aid rats in seeking social contact

Experiment-rats immobilized for 3hr w/ control odor (peppermint) or fear-associated odor (fox urine)
-if stress is too high, then cuddling and oxytocin increases a lot less than when stress is low-moderate
-> social contact may only be effective to allow allostasis but cannot prevent allostatic load

A

Kirby’s Research

74
Q

emotion enhjacnces memory
-proptanolol does not block memory (per se), blocking epinephrine receptors block stress-induced enhancement of memory for emotionally-laden material
-larger social network less likely person is to die

A

short-term stress in humans

75
Q

1) McGaugh’s work shows that small bursts of epinephrine is good for memory, so an acute stressor that releases epinephrine helps you to remember stressor and possibly avoid it in the future
-shown that blocking epinephrine receptors in brain does not alter memory but does block any enhancement of memory caused by an acute stressor
2) human demographic data show that social support buffers stress response
-> Kirby’s work shows that stress activates oxytocin release, which increases social boding
-indirectly, oxytocin may be a stress-reducing hormone

A

Revelations of McGough and Kirby Studies

76
Q

enhances memory
-presentation of small/weak shocks at time of red light makes it easier to remember that the red light signals food
-brief (3hr) immobilization stress increases hippocampal neurogenesis
-w/ one small dose of corticosterone, neurogenesis increases
-> cortisone or immobilization for 7-10 days, neurogenesis goes down in hippocampus

A

Short term stress in rats

77
Q

offspring of “high” grooming mothers are more resilient to stress as adult rats than offspring of “low” grooming mothers
1) means glucocorticoids return to baseline after a stressor more rapidly
2) means they have more glucocorticoids receptors in hippocampus and thus a better feedback mechanism for turning off of adrenal cortex response to stress
-> daughters inherit maternal licking and grooming behavior from mothers
–their babies (the grandbabies) are more stress resilient/have more glucocorticoid receptors in hippocampus, as stress resilience/vulnerability is inherited via maternal-side epigenetics
-low to moderate levels of stress are actually good for the body and brain while high/prolonged stress is detrimental
–high stress decreases hippocampal neurogenesis, memory, and lowers LTP
-small, short stressor appears to immediately increases neurogenesis, memory, LTP

A

Meaney experiment

78
Q

has done many studies to determine whether elevated glucocorticoid levels could accelerate brain aging
-through a negative feedback system, the hippocampus normally inhibits the release of more glucocorticoids
–thus, hippocampus is damaged-> increased secretion of CRH and consequently an increase in secretion of ACTH and hormones of adrenal cortex

A

Sapolsky

79
Q

removal of adrenals in middle-aged rats results in low levels of glucocorticoids
-prevents usual rise in serum glucocorticoids that typically accompanies aging
=> rats in old age = hippocampus do not lose as many neurons and lack common memory problems
-high levels of glucocorticoids may have damaging effects on neurons in hippocampal formation, leading to memory dysfunction

A

effects of glucocorticoids in old age

80
Q

1) dangerous to constantly mobilize energy at expense of energy storage
-breakdown of stored proteins in order to put amino acids and glucose into circulation produces myopathy and fatigue
2)cardiovascular problems
-increase in BP can damage heart muscle, weakening vessel walls

A

Evidence for Lack of Evolution for Chronic Stress

81
Q

-receptors for glucocorticoids in hippocampus exert (-) feedback control on hypothalamus and anterior pituitary and tells them to stop releasing CRF and ACTH so less adrenal cortisol is released
-stress response is not perfect–particularly not if prolonged or too freq or if it is, it is v. predictable

A

stress and negative feedback

82
Q

state of “living in chronic low level stressor and effectively dealing with it”

A

McElven’s allostasis

83
Q

improved memory at medium stress levels, poor at high stress
-testosterone secretion decreases
-growth hormone secretion decreases
-decrease interest in sex, decrease pain perception, increase water retention
-puts energy into blood, increase heart rate/breathing/BP/water retained
-curtails anabolic processes (digestion, sleeping)
-curtails reproduction, tissue repair, and growth
-suppression of inflammation and pain-stress induced amygdala

A

lots of glucocorticoid receptors cause….

84
Q

primary glucocorticoid in humans/primates

A

Cortisol (hydrocortisone)

85
Q

a hormone released by the hypothalamus that signals the release of ACTH by the anterior pituitary gland

A

corticotrophin-releasing hormone (CRH)

86
Q

steroid hormone secrets by adrenal cortex
ex-testosterone and estradiol

-cause a decrease in inflammation and act on brain on hippocampus where are lots glucocorticoid receptors

A

glucocorticoids

87
Q

outer later; secretes a class of steroid hormones-glucocorticoids and mineral corticoids
-capacity to respond to stress is one of the most basic mechanisms to mammals
-secretion of epinephrine and glucocorticoids by adrenal are 2 components of response
-epinephrine release is stimulated by nerve while glucocorticoid release is stimulated by a series of hormones

A

Adrenal cortex

88
Q

inner core; part of sympathetic NS
-receives direct neural input from the vagus
–therfore, it reacts v. quickly via APs in vagus to release epinephrine/adrenaline and norepinephrine into bloodstream
-hormones manufactured here

A

Adrenal Medulla

89
Q

-adrenal gland has two systems to deal with stress
1)Adrenal Medulla
2) Adrenal Cortex
-when stress is perceived via sensory input or imagined by cortex, sympathetic NS is activated immediately (w/in seconds) or epinephrine is released from adrenal gland
-> heart rate increase, blood pressure increases, digestion stops, etc
-CRH released from hypothalamus and stimulates pituitary gland to release ACTH (in 15s), which stimulates adrenal to release glucocorticoids (w/in a few minutes)

A

Two Stress Hormone System

90
Q

-1st to describe role of hormones in maintaining homeostasis in response to stress
-1st to emphasize connection btwn stress and disease
–suggested initial response to stress (alarm stage) is followed by 2nd stage in which successful activation of appropriate response system could re-establish homeostasis
–if stress is prolonged or freq repeatedly, the exhaustion phase occurs
–in this stage, there is increased susceptibility to disease
-Selyes model modified in light of recent work showing that common feature that characterizes “stressors” is their unpredictability or individual’s inability to cope with them
-therefore, something that is stressful to one individual may not be stressful

A

Han Selye contribution and model

91
Q

-coined “stress response”
-1st to describe imbalances in homeostatic system when stress occurs
-1st to realize the nonspecific nature of the response to stress
-> winner and loser are equally stressed/whether you flight or fight-> stress signals
-1st to point out important roles of hypothalamus and Autonomic nervous system in stress response

A

Cannon contributions

92
Q

combination of Cannon-Bard and James-Lange Theories
-like James-Lange, stress first produces physiological state
-like Cannon-Bard, it then suggest that we cognitively/emotionally label this new bodily sensation by looking around us and seeing what the change in sensation might mean
-two-factor theory

A

Schater-Singer Theory

93
Q

stress first activates physiological response, which leads to emotional perception of stress

A

James-Lange Theory

94
Q

stress leads to both emotional perception of stress (I feel stress) AND at the same time causes physiological markers of stress (ex-increased heart beat)

A

Cannon-Bard Theory

95
Q

how our body and brain (and behavior) respond to a stressor
-an adaptive response of body back to sort of homeostasis

A

stress response

96
Q

anything that creates stress

A

stressor

97
Q

anything that creates on imbalance or disturbance in homeostasis
-composed of stressor and stress response

A

stress

98
Q

initial drug uptake -> pleasure and wanting (cues repetition) -> incentive salience of wanting circuits-> parallel with tolerance/reduced pleasure -> increased consumption -> leads to compulsive drug taking (wanting/not liking) -> leads to cycle of relapse and disruption of lives -> abstinence/withdrawl -> drug assoc cues acts as potent triggers of craving and relapse (no cue for drugs in facility)

A

Addiction

99
Q

changes brain structure and function
ex-dopamine D2 receptors lower in addiction in NAc
-more synapses but less receptors in addicted brains
-as more dopamine appears, brain tries to establish homeostasis, makes more synapse
-regulates postsynaptic response with less receptors
-> explains tolerance-> need more drug for same effect
-> lowers want for food and sex-> drugs more pleasurable/potent
-dopamine starts in VTA and axons to various areas

A

effects of addiction

100
Q

binds to reuptake mechanisms and prevents reuptake
-leaves more dopamine in synapse

A

caffeine

101
Q

indirect change in dopamine
-inhibits GABA transmission in VTA, activating dopamine release in NAc

A

alcohol

102
Q

food and sex increase dopamine by 10-20% while drugs up to 200-1000%
-easier to become addicted due to pharmacological effect -> co-ops and overstimulates system

A

impact of drugs

103
Q

binds to opiate receptors in NAc, decreases GABA releases
-decreases GABA inhibition of dopamine release in VTA and NAc
-increases in dopamine leads euphoric/rewarding effects

A

morphine

104
Q

binds to Ach receptor
-A4B2 nicotinic receptor is in VTA after binding, leads to dopamine release in NAc

A

Nicotine

105
Q

1)competes with dopamine for dopamine transporter, inhibiting reuptake
2) displace dopamine from vesicles–dumps more dopamine into synapse
3)inhibits enzymatic breakdown of dopamine (MAD enzyme), increases synaptic dopamine by increasing release
4)binds to transporter and reverses it

-quick effect

A

amphetamine

106
Q

attaches to dopamine transport, blocking dopamine recycling
-dopamine remains in synapse longer
-continues to stimulate postsynaptic receptors
-slower effect

A

cocaine

107
Q

brain stimulation causes dopamine release here
-mesolimbic and mesocortical dopamine systems often seems surprisingly unable to alter basic hedonic reaction to pleasure
–in contrast to opioid and other true brain hedonic outputs that generate liking
-more wanting than liking -> incentive salience

A

ventral tegmental area and dopamine

108
Q

defined as want for something you neither like nor expect to like
ex-gambling, stalking

A

irrational desire

109
Q

VTA (amygdala, septum) sends axons to NAc sends axons to PFC

A

medial forebrain bindle

110
Q

necessary for repetition and memory formation
-involved in motivation, movement, addiction, and reward and wellbeing
-presynaptic vesicles release NT due to Ca2+ influx into synapse, binds to postsynaptic receptors
-can be recycled and repackaged (reuptake) by presynaptic transporters

A

dopamine

111
Q

pre understanding of liking vs. wanting

stimulus of NAc and/or VTA
-self stimulation reward, differs from natural reward in that no satiety/deprivation state, no neural representation to facilitate learning of reward expectancy (need reminder), want stimulation, compulsive behavior, no learned association btwn action and stimulation

A

Olds and Milner (1950s)

112
Q

regions of associative processing

A

amygdala and hippocampus

113
Q

regions of cognitive processing

A

orbital frontal cortex, anterior cingulate cortex, MPFC, insular

114
Q

EVIDENCE
-pleasure-generating capacity in NAc and ventral palladium have been revealed in part by studies in which microinjections and receptor-stimulating drugs into this region caused a doubling or tripling of number of hedonic “liking” reactions normally elicited a pleasant sucrose taste
-> if you drop opiates onto ventral pallidum or NAc, rats make more liking faces to a sucrose solution than when you drop saline or dopamine agonist into same region
-neuronal firing response from ventral pallidum; input from NAc, sends output to thalamus

A

subcortical liking

115
Q

hedonic (pleasure) cortex involves regions such as orbitofrontal, insula, medial, prefrontal, and cingulate cortices
-> studies have shown that the orbitofrontal cortex activity correlates strongly with subjective pleasantness ratings of food varieties, sexual orgasms, drugs, chocolate, and music
->subjective liking decreases, thus activity in your orbital frontal cortex decreases (ie with every bite)

A

cortical liking

116
Q

-if a rat is placed in an apparatus asked to press a lever for food, in initial training session, dopamine levels rise when rat gets food
-if a light precedes availability of lever and food over time, rat learns to associate light with eventual delivery of food
–soon light stimulates dopamine release, well before food is delivered
-if you then only make food available randomly after elver 50% of time dopamine levels will rise higher when light comes on
*anticipation is greater if reward is uncertain and overtime becomes rewarding

A

wanting experiment

117
Q

discovered that there were brain regions that, when stimulated electrically, could cause a rat (and even a human) to press lever/button to get stimulation
-> called “self stimulation reward” bc appeared that stimulation (firing AP) in these brain regions was rewarding
-further research showed that these regions were along mesolimbic and mesocortical dopamine pathway

A

James Olds (1940s-50s)

118
Q

stimulation (firing AP) in these brain regions was rewarding
-along mesolimbic and mesocrotical dopamine pathways
-discovered in James Olds
–not the same as food or sex: no satiety, must be reminded daily/no lasting association, no hedonic response to stimulation, causes pure wanting–no external cues so no warning

A

self stimulation reward

119
Q

-wanting without hedonic liking
-possibly how we develop irrational desires-> don’t like it or expect but keep doing it
ex-smoking, addictions, stalking, etc
-dopamine
REGIONS: NAc, ventral tegmental area, medial hypothalamus

cognitive process that confers “desire” or “want” attribute which includes a motivational component, to a reward stimulus-learning
-> cue is rewarding, triggering dopamine release

findings from both lever-pressing for food and sex and lever pressing for self stimulation reward have suggested that “wanting” (dopamine release) may increase attribution to surroundings and stimuli perceived at that moment, especially to eat of stimulating the electrode or to stimuli surrounding eating food
-if stimulation causes “wanting” attribution to button and that act of pressing it, people might well “want” to activate electrode again, even if it produced no pleasure sensation

A

incentive salience

120
Q

component of wanting
-dopamine
cortical regions: orbital frontal cortex, anterior cingulate cortex, insular cortex

A

conscious desires

121
Q

-several regions where learning about reward occurs
-all conscious cognitive learning occurs in cortical areas while learning association occurs in amygdala and hippocampus

A

Reward Learning

Psy 106 (3 decks)

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