1/64
Looks like no tags are added yet.
Name | Mastery | Learn | Test | Matching | Spaced | Call with Kai | Chat |
|---|
No analytics yet
Send a link to your students to track their progress
MPOA
medial preoptic area - responsible for male secual behavior
MPOA lesion
decreases male copulatory behavior
MPOA stimulation
increases male secual behavior
inject testosterone in MPOA
increases male behavior
VHM → PAG
ventromedial hypothalamus → preiaqueductal gray, responsibel for femal secual ehavior
VHM lesion
decreases stimulation
inject estrogen in VMH
increases female secual behavior
C&R without early T
female typical beahvior (regardless of genotype)
C&R early T
male typical behavior (even in genetic females)
C&R high does E in females
can also masculanize (aromatzation to T)
male typical behavior requirements
early ORGANIZATION (permanent wiring) + Later ACTIVATION (hormone trigger)
organizational/activational hypothesis
permanently hard wires the brain circuits for male and female typical behavior/hormones switch on/inhibit/modulate the already built circuit
kinefelter syndrome XXY
extra x, small testes, low testosterone, often tall, some breast development, usually infertile
androgen insensitivity (CAIS)
XY w/x linked mutation → the testes make testosterone but nonfunctional androgen receptors cant responds it, normal female development except no uterus
XYY
taller than avg, usually normal secual development, IQ normal; mild learning language deficts
5a - REDUCTASE DEFICIENCY
cannot convert testosterone to DHT. male with ambiguous genitalia or undervirilization at birth.
turner syndrom - xo
one sex chromosome is missing. phenotypically female but ovaries are underdeveloped and non functional
DES exposure
synthetic estrogen exposure leading to reproductive tract abnormaalities and risk of vaginal cancaer
CAH
The adrenal cortex overproduces androgens. masculinize externalgenitalia
dimensions of biological sex
chromosomal sex → gonadal sex → hormonal sex → morphological sex → behavioral sex
LH lesion
complete lack of feeding (aphagia)
LH electrical stimulation
overeating (hyperphagia)
VHM lesions
hyperphagia + extreme obesity
VMH electrical stimualtion
aphagia
glucostatic/glucose utilization
short term (meal to meal)
lipostatic
long term (body weight control)
brown fat
burns calories as heat
white fat
main energy store
STM (primary memory)
short term, does not require protein synthesis
LTM (secondary memory)
long lasting, requires protein synthesis
results of LTD
AMPA receptor removed from membrane → nerve cell becomes less responsive to glutamate
synaptic plasticity
potentiation
increasing the probability of a long term effect
Early Long term potentiation
short lasting, no protein synthesis, relying on post-translational modifications
late long term potentiation
long lasting, requiring protein synthesis and gene exppression, involving changes in synaptic structure
long term depression
a process of synaptic weakening that decreases the strength of synaptic connections/ remove unnecessary connections, promoting efficent neural network organization
Basic Associative learning
learning about causal relationships in the world
S-S (stimulus stimulus) association
part of pavlovian conditioning; when two stimuli occur together, they become linked (ex pavlovs dog/salivary)
S-R (stimulus response) association
assc. w/instrumental conditioning, when a stimulus is followed by a response that results in a pleasurable outcome, they become linked
law of effect
behaviors followed by pleasant consequences are more likley to be repeated, while behaviors followed by unpleasant consequences are less likley to be repeated
positive reinforcement
R is followed by pleasurable stimulus (reward) → increase R
Positive punishment
R is followed by good/aversive stimulus → decrease R
Negative Reinforcement
R is followed by omission of aversive stimulus → increase R
Negative Punishment
R is followed by omission of reward → decrease R
Shaping
reinforcing successive approximations of a desired behavior until the target behavior is achieved
Delay condiitoning
when CS and US temporarily overlap
Trace conditioning
when there is a gap between the CS and US
trace interval
condiitoning gets weaker as interval gets longer
IP (cerebellar lessions)
abolish CR acquisition and retention
left cerebellar lesion
affects left eyeblink conditioning
right cerebellar lesion
affects right eyeblink conditioning
dementia
umbrella term to describe decline in cognitive function
early onset AD
age 30-64, 0.11%
Late onsent AD
65-74 (5.2%) 75-84 (13.8%) >85 (35.8%)
diagnosis of AD
amyloid plaques and neurofibrillary tangles in brain tissue, neurological exam