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87 Cards in this Set

  • Front
  • Back
NMDA receptors high in which area of the hippocampus
Right hippocampus
spatial, pictures
Left Hippocampus
Role of Hippocampus
incorperate context into memory
what part of brain lights up when ppl are going the explicit memory test?
Left hippo
Explicit =
word completion
Korsakoffs Syndrome
severe anterograde amnesia, confabulation, chronic alcholics
Korsakoffs Syndrome caused by what
deficency in thiamine B1
alcohol affects thiame absorption... and the dont get it in the diet
Damage in Korsakoffs
mamillary bodies and connections to thalamus (MAMMILOTHALAMIC TRACT)
- hippocampus and fornix
DAMAGE- korsakoffs
prefrontal cortex
Structures involved in memory
Hippocampus and its inputs and outputs
INPUT = entorrhinal cortex
OUTPUT = fornix
Damage to the prefrontal cortex leads to..
confabulation and damage to working memory (short term)
Structure involved in emotional Learning
Amygdala - conditioned emotional response
independent variable..
dependent varibale
indep = lights .. red -horn
depend= dev of conditioned emotional response
episodic memory
damage to the amygdala = impaired conditioned emotional response - no skin conductance. but could tell you what happened
damage to hippocampus
impairment to the recall.. but had skin conductance
Structures involved in Implicit memory
Cerebellum - sensorimotor skills
Implicit memory
striatum - memories for stimulus response
what are short term satiety signals
food being absorbed
what are long term satiety signals
signal from adipose tissue about long term nutrient resevoir
modulates sensitivity of brain areas involved in hunger
what is the short term satiety signal from the duodenum?
what are the functions of CCk
cause gall bladder to release bile
inhibits stomach contractions
sends signal to brain via vagus nerve
what is CCk
a peptide hormone
released in response to fats
what axons from duodenum are sensitive to glucose, aas, and fa;s
entry of food into the duodenum .. causes you to eat more or less
Short term satiety signal
signals from the liver continue the satiety started by duodenum
study with dogs
glucose injected into the portal vien vs jugular vien
long term satiety signal.. study with ob mutant mine
they got fat
long term satiety signal
LEPTIN.. from adipose tissue
in the 1950s and 1940s it was first hypothesized that if the Lateral hypothalamus was lesioned
then you would stop eating and drinking
in the 1950s and 1940s it was first hypothesized that if the ventromedial hypthalamus was lesioned
then it would disrupt ANS and cause increased eating = obesity
what are the names of the 2 neurons that play a role in stimulating hunger and decreasing metabolism in Lateral Hypothalamus
Melanin concentration hormone
orecin A
cells that produce MCH and orexin project to areas invloved in (3 things)
movement and metabolism!!!
Non Exercise Activity Thermogenesis
NEAT - aka fidget factor - always moving
Is obesity caused by a faulty gene?
Sensitivity to leptin?
difficult to get across the blood brain barrier
Leptin and Obesity Blood levels =?
Blood ratio = 318%
CSF ratio = 30%****
uncomfortable fulness
Treatments to obesity
Serotonin agonists - increase the release of serotonin "Fen Fen" increase risk of heart attack supress eating
supress eating
Anorexia - only ___% recover
are anorexics just not hungry?
no becuase they are still secreting insulin in the presence of food
Brain changes in anorexia
- enlarged ventricles and sulci
After stopping anorexia
ventricles do not return to normal.. sulci do!
Neuropeptide Y in CSF is elevated while anorexic T or F
Leptin is high or low when anorexic
LOW - little fat cells, it also returns to normal before weight does.. therefore its hard to reach normal weight
anorexia Drug treatments
Cyproheptadine (antihistamine + antiserotonergic drug)

Bulimia = fluoxetine (prozac)
TOools to investigate sleep
name 3
electroencephalogram EEG
electromyogram (EMG)
electrooculogram (EOG)
EEG patterns
Awake - ____ waves
BETA waves
Awake - Relaxed or eyes closed
___ waves
ALPHA waves
brain processing less infor
Sleep - stage 1
transition between sleep and wakefullness
-theta activity
-10 mins

eyelids droopy .. head nodes
Stage 2
theta acvitity
Sleep spindles - ignore noise from external environment
K Complexes - make less sensitive to noise - once asleep stay asleep
- 15 mins
Stages 3 and 4
slow wave sleep
delta activity
cerebral blood flow decreases
hard to wake people, groogy
thoughts, images and nightterrors , somnambulism
sleep walking
REM / Dream Sleep/ Paradoxial Sleep
desyncronyzed EEG (resembeles alertness)
Genital Activity
REM - rapid eye movemetns
forget about dreams fast
no muscle movement
increased blood flow in cerebral blood in visual association areas
DECREASED cerebral blood flow in frontal cortex
First half of the night.. more in what sleep.?
slow wave sleep stages 3 &4
Second half of the night .. more in what sleep//
REM sleep
less deep sleep
Slow wave sleep - deep sleep
Experiments - treadmill
museum and hairdryer
exercise experiment
25% more time in deep sleep than the ppl running infront of the fan
recovery from intense mental activity
increased slow wave sleep
increased slow wave sleep
slow wave sleep increased b/c...
brain need to recuperate.. brain metabolism ..
release of growth hormone
healing the body
paropologixs - cannot move but still spend time in slow wave sleep
circadian rhythm
purpose to avoid predators?
dude that slept a lot
didnt catch up on sleep hours but slept more in deep sleep less in stage 1 and 2
REM sleep
memory consolidation
flushing of useless info
rem rebound
someone deprived of REM sleep - then allow them to sleep - they will spend more time in REM sleep
FXNS of REM sleep
brain development!!!
more developed brain..
less REM sleep
as a rodent learns something.. they have
as this becomes consolidated into LT memory
they decrease REM sleep
sleeping disorders
sleep apnea
REM with Atonia
Problems with Slow wave sleep
25% of pop
9% regularly
when you are awake you dont feel well rested
what isthe cause of insomnia
sleeping meds
tolerance and withdrawl
imsonmia cannot be treated with medications
insomnia is usually a...
SYMPTOM! treat ofther stresses first..
treatmesnts - insomnia
keep a regimented lifestyle
- sleep same amt everynight
- schedule
- no caffeine or alcohol
sleeping pills
go to bed 15 mins earlier - sleep extra 30 mins
- vallum- not well rested
tolerance andwithdrawl - must incrase dose for same affect
sleep apnea
- cessation of breathing while sleepign
- ppl always tired
co2 biuilds up - chemoreceptors - breath - wake up breath - fall asleep
treatment for sleep apnea
cause - obstructed airway
- relaxation of soft tissue= stop breathing
Treatment - diet and exercise
speciallty pillows
pressurized air mask
- more commone when on BACK
sleep apnea
more common in males. older ppl. obese
numbness seizure - sleep at inappropriate times
sleep attack - irresitable urge to fall asleep
cataplexy - down stroke.. REM sleep - paralyzed so muscles dont work
sleep paralysis
sleep paralysis
hypnogogic (GOING to sleep) or hypnopopic (WAKING up) hallucinactions
Narcolepsy causes
mutation in gene for orexin B receptor
skip slow wave sleep - directly to REM
stimulants - eg ritalin
catecholamine agonists(noradren, seratonin) (INCREASE RELEASE OF NORAD AND SEROTONIN)
drugs that act of orexin B receptors
REM without Atonia
lack of paralysis when asleep in REM sleep
inherited disorder
caused by damage to the regions of the reticular formation that inhibit movement
TREATEMENT = Drugs (bexoldiazephines) - vallium
PROB with slow wave sleep
commonly seen in children
nocturnal enuresis
pavor nocturnus (night terrors)