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203 Cards in this Set
- Front
- Back
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learning
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relatively permanent change in behavior as a result of event
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memory
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ability to recall or recognize previous experience
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engram
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ckarl lashley's phys representation of memory in brain; never found
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what part of brain did lashley remove that disrupts memory?
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none; only found that amt of cortex removed is important
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what parts of brain did HM have removed?
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hippocampus, amygdala, adjacent cortex
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anterograde amnesia
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inability to consolidate new memories into long term memory
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what type of memory did hm retain?
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procedural memory; temporal lobe amnesia
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name two types of declarative memory; define
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semantic: i know what a piano is
episodic: i remember buying that piano |
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procedural memory
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ability to learn tasks; i know how to play that piano
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consolidation:
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ability to turn new info into long term mems
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2 destructive forces in alzheimers disease
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beta amyloid plaque, neurofibrillary tangles from tau protein
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beta amyloid plaque is..
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toxic to neurons; extracellular damage
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tau protein forms...
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neurofibrillary tangles, aka tau clumping together
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what is brain atrophy? where does it occur?
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loss of neuron in cortex, hippocampus, and basal forebrain
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energy usage in alzheimer's patients?
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greatly reduced, duhh
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two current alzheimer treatments
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NDMA blockers (memantine)
acetylcholinesterase inhibitors (exelon) |
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side effects of exelon
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nausea, vom, poop, etc
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side effects of memantine
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anxiety
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hebb's postulate:
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learning is mediated by changes in synaptic strength or efficiency
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who studied learning in invertebrates?
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Eric Kandel
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species used for memory study? why?
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aplysia; had simple NS but same NTs and same APs
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what behavior in aplysia was studied? why?
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gill withdrawal reflex; mediated by single circuitry
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define habituation:
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decreased response to repeated innocuous stimuli
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example of habituation in aplysia
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ciphon touched with paintbrush, stopped retracting gill so strongly, if at all
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biological effects of habituation? why important?
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less NT transmitted; first time phys change in NS
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define sensitization, give ex
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stimulus followed by trauma = stronger response; aplysia stroked and had tail shocked, increased NT released
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what is long term potentiation?
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(lab created) burst of intense stimulation, leaves synapse potentiated for mins-wks
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where is it easiest to induce ltp?
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hippocampus
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what is the intent of studying LTP?
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measure change in efficiency in neuron
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LTP acts on what receptors?
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NDMA receptors (normally blocked by magnesium) and AMPA receptors (normally let in sodium)
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explain role of AMPA receptors in LTP
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when repeatedly stimd, Na depolarizes membrane which displaces magnesium; Na and Ca then enter through NMDA channels
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Receptors roles are maintenance and induction in LTP. Which does wiich?
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NDMA responsible for maintenance only; AMPA responsible for both maintenance and induction
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what can LTP do?
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make new connections or strengthen them
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LTP increases what type of receptors?
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AMPA, ya silly goose
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long-term depression
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prolonged decrease in response to synaptic input following low levels of stimulation (depotentiated)
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what happens when you block NMDA receptors in learning?
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hard to induce ltp; learning impaired
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what happens when Ca channels are blocked in LTP?
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LTP is prevented, learning difficult
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what are Doogie mice?
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mice breed to have lots of NDMA receptors; a little smarter, able to induce ltp easier
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what are hormones?
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chemical messengers secreted by endocrine glands into the bloodstream that act on target tissues throughout the body
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what are target tissues?
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cells with receptors that respond to only the hormone molecules that act on them
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difference btw NT and H?
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NT are released more locally, H travel throughout body
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similarity btw NT and H?
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both chem messengers that carry signals btw cells and act on specific receptors
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what are steroid hormones derived from?
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cholesterol
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three main types of gonadol steroid H
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androgens
estrogens progestins |
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main secreters of H
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gonad
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what do steroid Hs affect? for how long?
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gene expression; diverse and long lasting effects
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action of steroid H
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readily enter cell (fat soluble), bind to receptor in nucleus
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gonads
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ass and titties... jk ovaries and testes
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sex limited genes
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genes activated by androgen and estrogen
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differences in sex limited genes? examples..
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effects of H stronger in one sex than other; estrogen = breast devel, androgens = facial hair
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name three major classes of Hs and their major H
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androgen - testosteron
estrogen - estradiol progestin - progesterone |
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who is in charge, hypothalamus or pituitary?
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psh, gimme a break.... hypothal!
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where is gonadotropin released from?
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anterior pituitary gland
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2 gonadotropins released into general circuit; what do they effect?
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FSH and LH; effect gonads
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why is gonadotropin releasing H hard to study?
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very brief peptide Hs
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what is the portal system?
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closed circuit of bloodstream, self contained
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where does the portal system exist?
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between anterior pituitary gland and hypothal
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two types of receptors gonads have most of?
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FSH and LH receptors
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what are organizational effects?
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action of hormones during a sensitive stage of development that alters tissue differentiation
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how long do hormonal effects last?
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almost permanent, last even when H is no longer present
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when do organizational effects of H occur in humans? rodents?
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4 months prenatally for humans, few days after birth for rodents
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at how many weeks post-conception do M and F still look identical?
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6 weeks
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what are the precursors to gonads?
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primordial gonads
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precursor to internal f reproductive orgs?
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mullerian ducts
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wolffian ducts
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precursor to male repro orgs
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y chromosome triggers synthesis of?
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h-y antigen
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h-y antigen triggers?
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devel of testes
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what two things do testes release?
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mullerian inhibitor H and androgens (testosterone)
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during prenatal devel, testosterone released from testes triggers what?
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development of Wolffian ducts
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androgens released from testes trigger what?
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devel of EXTERNAL male sex orgs
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in fem devel, why are H-Y antigens not synthesized?
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no Y chromosome to trigger it
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why do ovaries develop in females?
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no H-Y antigen to trigger synthesis of testes; ovaries are default
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why do mullerian ducts develop instead of wolffian ducts in females?
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no testosterone is around to induce devel of wolffian ducts, no testes to produce mullerian inhib H
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absence of what H causes f ext orgs to devel?
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androgens
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what characterizes androgen insensitivity syndrome?
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lack of androgen receptors on cellular level
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ppl with androgen insensitivity syndrome: genetically m or f? int orgs = ? ext orgs =?
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genetically male, XY; int orgs male, ext orgs female. super feminine appearance
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in androgen insensitivity syndrome, why doesn't testosterone do anything?
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no androgen receptors, so even though testosterone is present, it doesn't do anything
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what characterizes congenital adrenal hyperplasia?
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adrenal gland produces large amounts of androgen during development
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congenital adrenal hyperplasia affects males or females?
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female! just gives males lots of testosterone. gross.
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what happens to female body in congenital adrenal hyperplasia?
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completely masculinized in appearance and "behavior"
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congenital adrenal hyperplasia: genetically m or f? int orgs? ext orgs?
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can be either (but condition affects f more, so focus there) XX or XY, int orgs of XX are female; ext orgs of XX are somewhat/totally male
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most common cause of ambiguous genitalia is?
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congenital adrenal hyperplasia
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what characterizes 5-alpha reductase deficiency?
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deficient of 5 alpha reductase so testosterone cannot be converted into DHT androgen
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what does DHT do?
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causes male orgs to look male
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people affected by 5-alpha reductase m or f? int orgs? ext orgs?
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males, int orgs are male (?), ext appears female at birth
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are the affects of 5 alpha reductase deficiency permanent?
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no, in puberty testosterone is main component so penis will develop
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t/f: m have more corpus callosum connections
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false, females do
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differences in brains btw f and m include:
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size (m 15% larger), diff vols of nuclei and tracts, diffs in number and types of synapse
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in rats 1 day old, what happens when you transplant gonads?`
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rat will grow up and function as opposite sex
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what is monitored to see the effects of gonad transplants?
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FSH and LH neutrotrophins; f pattern = cyclical, m pattern = constant
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what have studies attributed brain gender to?
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testosterone
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nucleus of medial preoptic area diffs btw m and f:
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bigger in m
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what happens if you castrate a male rat on day 1?
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female like brain!
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what can cause permanent reorganization in the brain?
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hormone exposure during sensitive devel period
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what controls female sexual behavior?
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ventromedial nucleus of hypothal via projection to periaqueductal gray
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what controls m sex behavior?
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medial preoptic area via projection to lateral tegmental field
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what is responsible for masculinization of rat brains?
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estradiol aromatizes testosterone
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if f rat is injected with estrogen on day one, what happens?
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brain is masculinized
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what happens if f rat is injected with DHT on day one?
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nothing; estrogen masculinizes female rat brains
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what prevents f brains from masculinization in womb?
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alpha fetoprotein in babies bloodstream binds to estradiol, making molecule too big to pass blood brain barrier
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why are m able to develop into m brains if alphafetoprotein is floating around to stop all the estradiol?
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testosterone can cross blood brain barrier and become estradiol on the other side
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if you injected a female rat with estradiol could she be masculinized?
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yes, because theres a limited amount of alphafetoprotein
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two reasons why aromatization is not necessary in humans:
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testosterone can directly masculinize brain, and estradiol is capable of masculinizing brain
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how are human fs protected from estrogen in womb?
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placental barrier protects baby when it is delivered from estradiol
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what were side effects of synthetic estrogen (IDES)? why was it given?
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given to prevent miscarriage, but masculinized f brains partly, and f baby had an increased rate of homosexuality
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other mechanisms in sexual development:
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sex chromosome maybe, and thats it really, we have no idea
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what are the activational effects of gonadal hormones?
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action of hormones in adults that usually only last while hormone is present
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what happens if you give a castrated male rat testosterone?
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sexual interest returns
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when is sexual peak in human males?
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teens-25
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when does female initiated sex peak? for women on birth c?
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ovulation; same across month
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when ovulating, what face does woman pick? when not?
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masculine during ovulation, feminine during rest of month
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list main differences in activational effects across orientation:
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none, fool!
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% of gay m with identical gay twin
% of gay m with frat gay twin |
50%, 22%
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explain the fraternal birth order effect
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for every male older brother, likelihood of homosex is 30% increased
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what is maternal immune hypothesis?
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mom develops immunity to androgens, the more boys the stronger the immunity, androgens become less effective
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brain diffs between straight/gay
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dimorphic nucleus of the hypothalamus halfway btw m and f.... NOT!
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biological clock... how long?
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internal time keeper driving rhythm, about 25hrs
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free running rhythm
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studied by frenchman in cave for 7 months, occurs when enviro cues are absent
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zeitgebers
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stimuli for keeping bio clock on time
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main zeitgeber? other zeitgebers?
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light!
food, activity, sound |
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what occurs when bio clock and external clock are at odds?
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jet lag, late shifts, all that junk
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if this part of your brain is lesioned, circadian rhythms are messed up:
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superchiasmatic nucleus of the hypothalamus
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where is the superchiasmatic nucleus of the hypothalamus located?
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above the optic nerve
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name two circadian genes
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CLOCK and tau
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what do circadian genes do and what are they affected by?
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transcribe proteins that regulate rhythms; affected by light
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where does direct communication between the superchiasmatic nucleus and retina occur?
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retinohypothalamic tract! silly goose.
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what happens if the optic tract is cut?
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rat is blind, but circadian rhythms are not disturbed, sleep pattern is fine
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what happens if the optic nerve is cut?
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rat is bling, circadian rhythms interrupted
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where does input from the superchiasmatic nucleus go to? what does it do?
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pineal gland; regulates release of melatonin
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other areas of brain that have to do with sleep cycles?
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thalamus
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what does an electroencephalograph do?
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graph of brains electrical activity
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what does EEG display?
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displays average of all neuron potentials; waves measured in hertz
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initial stage one of sleep
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hr brain activity and breathing slow.
brain waves are low voltage and irregular |
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sleep stage with brief burst of rapid waves and high amplitude waves
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stage 2
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sleep spindles
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rapid waves
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k complexes
purpose? |
high amplitude waves
block out stimuli maybe? |
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stage of sleep characterized by slow waves
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3 and 4
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>50% alpha waves
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stage 4
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<50% alpha waves
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stage 3
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at what stage is input to cortex greatly reduced?
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stages 3 and 4
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speed of slow waves in 3 and 4
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1 to 2 hertz
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REM stage and emergent stage 1
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irregular fast waves, indicating lots of brain activity
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when does most rem sleep occur?
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second half of night
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when sleep intrude on wakefulness
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narcolepsy
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when wakefulness intrudes on sleep... cycle?
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lucid dreams; REM
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cataplexy
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muscle weakness, similar to in REM
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hypnagogic hallucination
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dreamlike experiences while falling asleep
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what causes REM behavior disorder?
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damage to pons
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what characterizes REM behavior disorder?
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not being paralyzed during REM
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fatal familial insomnia
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stop being able to sleep, kills you within 5 months
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what causes FFI
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damage to thalamus
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where does arousal happen in brain?
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pontomesencephalon
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excitatory connection to basal forebrain
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reticular formation
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what does the reticular formation do?
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elicits arousal
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why is it hard to recall dreams?
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locus coerculus is completely inactive during sleep, thought to be important in storing memory for important events
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what emits bursts of norepinephrin during meaningful events?
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locus coerculus
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where is the locus coerculus located?
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pons
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major source of excitation and inhibition to cortex
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basal forebrain
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what is adenosine monophosphate broken down into?
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adenosine
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when are adenosine levels highest?
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at night
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neurons that have adenosine receptors produce what?
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ACh
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what is the action of adenosine on ACh producing cells?
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inhibitory
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what does caffeine do to adenosine?
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caffeine inhibits adenosine! aka it is an antagonist at the adenosine receptors
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where do a separate population of inhib and excitatory cells live?
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hypothalamus
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excitatory arousal system
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histamine
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why do antihistamines make you drowsy?
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they block histamine, the excitatory arousal system in hypothalamus
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good predictor of how fast you fall asleep
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decrease in body temp
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where does activity increase as you enter rem?
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pons
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how is muscle activity shut off in rem?
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signal from pons to spinal cord
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waves characteristic in REM? direction traveled?
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pons geniculate occipital waves; travel up
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support for recuperation theory:
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if we don't sleep we die
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recuperation theory:
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body and brain need to repair after day's activities
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circadian theory of sleep
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sleep because of our internal clocks and it is safer
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evolutionary considerations
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every mammal and bird sleeps, regardless of size, temp, activity
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what happens in rem cognitively?
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memory storage, consolidate info
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what is rem rebound?
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spending more time in REM when REM deprived
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why do we dream?
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cortex is active because of pons signaling, so brain is aroused and ready to process, but there's no external input; focuses on memories instead
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dream theory
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activation synthesis hypothesis
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what happens when brain perceives stressor?
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neural pathways activate hypothalamus
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what two systems do the hypothalamus activate when stressor is perceived?
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sympathetic and parasympathetic
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which division of autonomic NS activated first when stressor perceived? what does it do?
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sympathetic; increases HR and blood press, increased release of epinephrin and norepinephrin
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where are epinephrin and norepinephrin released from when sympathetic NS is activated from stressor?
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adrenal medulla
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what is the HPA axis?
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hypothalamus pituitary gland adrenal cortex.
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what is ACTH?
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adrenocorticotropic hormone
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how is ACTH released? where does it go?
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ACTH is released when the hypothal acts on the anterior pituitary gland; ACTH then acts on adrenal cortex to cause release of glucocorticoids
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what causes release of glucocorticoids?
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released by ACTH acting on adrenal cortex
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main glucocorticoid?
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cortisol
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most common physiological measure of stress?
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cortisol in saliva
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why do stressors elicit same phys response?
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need to mobilize energy fast!
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during stress, energy is needed. what happens?
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energy storage is inhibited, and existing stores are broken down into readily used forms
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what is elevated in blood when energy stores are being broken down under stress?
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elevated levels of oxy and glucose in blood
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when does stress reaction become maladaptive?
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prolonged activation, or not activated for phys reason
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health issue associated with stress
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gastric ulcers
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theories of gastic ulcer causes?
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stress, H pylori, both + ibuprofen
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problem with H pylori theory of ulcers?
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70% people without ulcers have bacteria
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psychoneuroimmunology
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study of interaction btw immune response, psychological factors, and NS
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brief stress effect on immune system? prolonged?
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brief = boosts! prolonged = harmful
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why is prolonged stress bad for immune system?
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unclear. but cells involved have lots of glucocorticoid receptors
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Yerkes dodson curve
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arousal measures, apply to stress as well; optimal levels
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hippocampus has high levels of what receptor?
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corticosteroid receptors
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type 1 vs type 2 corticosteroid receptors
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slight activation of type 2 is optimal, too much is bad for memory
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what causes damage to hippocampal cells? how does that damage manifest?
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chronic activation of corticosteroid receptors; fewer dendritic spines, broken, thinner
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dendritic spines from where are damaged when there is chronic activation of corticosteroid receptors?
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pyramidal neurons!
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