NSC 2201: Final Exam Review
Terms in this set (90)
process whereby we acquire new information about the world
a process whereby we retain that information over time
What are difference between learning and memory?
learning = acquiring new info = molecular problem
memory = pulling that info out again = molecular + systems problem
What is declarative memory?
being able to declare something as a fact
i.e. your birthday, date of WWII
What is non-declarative memory?
processes you implicitly can do
i.e. playing piano, emotional responses, moving around
i.e. phone number
short term memory
minutes / hours
i.e. repetition of name
is forgettable - might not remember the next day
long term memory
dates, months, years
i.e. remembering sister's name
What invertebrate model was used?
California sea slug (aplasia californica)
What are the advantages of sea slug model?
nerve cells form same, reproducible circuits in every animal
ability to learn
learning to ignore stimulus
learning to intensify a response to stimulus that previously evoked no reaction
non associative learning:
anything that is not classical conditioning - i.e. not forming an association
habituation & sensitization
classical conditioning - association a stimulus that evokes a measurable response (US) with a second stimulus (CS)
What learning occurred with the slug?
repeating stimulation of siphon => less contraction of Gill Muscle
repeated stimulus -> response weakens
What is the molecular basis of habitation?
less Ca2+ => less contraction
therefore, less calcium => less withdrawal of gill muscle = habituation
What causes sensitization in the gill muscle?
i.e. electronic shock of gill => increased response than normal
What are the steps of sensitization?
electrical shock applied
5-HT is released presynaptically by L29 onto sensory neuron
GPCR is activated by 5-HT => activates adenyl cyclase => produces cAMP => activates PKA => closes K+ channel => prolonged AP => more Ca2+ entry => more NT release
What is the short-term info about sensitization?
5HT => activates PKA => more Ca2+ => more NT release
What are the US, R, and CS or gill reflex?
US = strong shock of tail
R = withdrawal of gill
CS = gentle stimulation of fsiphon
What is the similarity between sensitization and classical conditioning?
both involve PKA -> increased NT
What is the difference between sensitization and classical conditioning?
sensitization = serotonin
classical condition = calcium and serotonin
What changes occur in vertebrates and invertebrates?
invertebrates = presynaptic changes
vertebrates = postsynaptic changes
Hebb's rule #1:
neurons that fire together wire together
learning = synaptic strengthing
coactivation of pre and post synaptic neurons
Hebb's rule #2:
neurons that fire out of sync lose their link
forgetting = synaptic weakening
presynaptic axon is active, but postsynaptic axon is WEAKLY activated
What determines remembering vs forgetting?
level of postsynaptic activation
What induces LTP?
high frequency stimulation
What induces LDP?
low frequency stimulation
ligand gated, conducts Na+
ligand and voltage gated, conducts Na+ and Ca2+
What do AMPA and NMDA receptors both respond to?
both respond to glutamate
you need both receptors to have LTP
How do AMPA and NMDA work in LTP?
Glutamate binds to AMPA and you get Na+ influx
When you get enough Na+ to reach threshold, Mg2+ is bumped off NMDA receptor
Then get Ca2+ and Na+ flowing thru
Ca2+ entry triggers both LTP and LTD
What does the level of Ca2+ entry indicate?
high freq stim => more Ca2+ => protein kinase => LTP
low freq stim => less Ca2+ => protein phosphatase => LDP
therefore, the level of Ca2+ determines whether you have protein kinase or protein phosphatase which determines LTP vs LDP
what changes occur in short term memory?
-phosphorylation of AMPA receptors
-externalization of AMPA and NMDA receptors
-synthesis of more receptors (adding more strengths memory)
What changes occur in long term memory?
pre and post synpatic
=> happens at
level of protein synthesis
Morris Water Maze:
used to test mice memory
has to remember platform below water surafce
if you take out hippocampus, mouse will have no clue where the stage is
simultaneous EPSPs from multiple synapses (summation)
neurons will be strengthened as you have more activation
more input = stronger activation
What are predispositioning factors to depression?
family history of depression (genetic)
childhood neglect or abuse
What are the two types of major depressioN?
-stable down mood
anorexia = weight loss
*HPA axis dysufnction
-increased central drive
-increased CRH, ACTH, cortisol => no feedback inhibition*
variable hedonic response
hyrerphagia = weight gain
HPA axis dysufnction
decreased central drive
difference in response to stress in normal individuals and depressed individuals?
Normal individuals bounce back from stress whereas depressed individuals don't bounce back
What happens with high levels of cortisol and the hippocampus?
hippocampus is very responsive to high cortisol levels and shrinks
What does the diathesis-stress model state?
predispostional vulnerability + stress > threshold = depression
What happens to hippocampus in depression?
antidepressants stop this by increasing 5HT, NE, BDNF and GRs
What are the treatments for depression?
What are antidepressants ultimately thought to do?
increase GRs and BNDF
allows hippocampus to better suppress HPA axis
positive symptoms of SZ
positive symptoms = increased levels of something
grossly disorganized or catatonic behavior
negative symptoms of SZ
negative symptoms = decreased levels of something
reduced emotional expression
poverty of speech
etiology of SZ slide:
selective cell death
Weinberg DA hypothesis of SZ
start of SZ = decrease in dopamine
decrease in DA => decreased activation of prefrontal cortex => less inhibition of brainstem => increased activation of nucleus accumbens => positive symptoms
decrease in DA => decreased activation of prefrontal cortex => negative symptoms
What does Joseph Coyle's Glu hyptoehshs o SZ state?
glu = major excitatory NT in brain
-regulates pruning of excess neurons
-NT released during LTP
Glu acts thru NMDA receptor to decrease both positive and negative symptoms
suggests that Glu dysregulation may occur in regional subpopulations of the brain of SZs
bottom line: in SZ, there is a sub-sensitivity of the NMDA receptor which is activated by Glu
What mental illness is the highest with familial inheritance?
What are the two types of addiction?
natural -> food, water, sex, nurturing, socializing
artificial => drugs, money, gambling
What do addictive drugs cause?
release of dopamine at nucleus accumbens
dopamine activates GPCRs
What are new insights into the role of DA?
of dopamine plays important role => faster rate = more intense reinforcing effects
long-term drug abuse
decreased DA function
What do stimulants do?
cocaine, amphetamine, methampheamine
block the dopamine and NE transporters
How is ADHD treated?
treated w/ stimulants => Ritalin and adderal
dopamine transporters work in reverse in ADHD
in normal individuals, Ritalin and adrenal increase APs
in ADHD, ritalin and aderla decrease Paps
goal of treatment: to restore optimal levels of NE and DA
ecstasy / MDMA:
higher affinity for SERTs than serotonin
reverses the SERT => pumps serotonin into synapse
long term can cause loss of 5HT axons and terminals
What can MDMA cause ?
depression and anxiety
also obsessive traits, paranoid thoughts, disturbed sleep, substance abuse disorder, memory impairment
benzodiazepines barbiturates alcohol opiates
What do depressants do?
activates GABA receptor and causes Cl- to flood in, decreasing number of action potentials
benzodiazepines - GABA co-agonist => has different binding site rom GABA so can have addictive effects
opiates - GABA agonist => binds to same site
What does fentanyl do?
fentanyl = heroin additive that causes overdose => makes GABA Receptor much more active
Why is the brain vulnerable to disease?
no cell division in neurons after birth
unique blood supply
physical location - any space occupying mass is life-threatening
Swelling brain can go thru ______________
foramen magnum => hole in base o skull thru which the spinal cord passes
lack off blood flow to brain which causes lack o oxygen
= main risk factor
higher stroke risk in women than men
symptoms occur rapidly
What are the different types of stroke?
1. occlusive stroke = blockage
2. hemorrhagic stroke = bleed
What are infarct and ischemia?
infarct = dead neurons
ischemia = damaged neurons => penumbra
-neurons that need to recover
infarct causes ischemia => too much Ca2+ flows thru NMDA
Why is there increased risk after first confusion?
brain hasn't completely healed from first consussion
any impact causes much greater
-K+ efflux, Glu release, Ca2+ thru NMDA receptors => excitatocity
progressive degenerative brain disease seen in athletes with a history of repetitive brain trauamaQ
What are brain tumors?
collections o new cells in the brain
classified by histological appearance
two major classes
brain tumor facts:
brain radiation =
#1 risk factor
is VERY important
of tumor is most important characteristic in determining prognosis
prognosis for patients with astrocytomas
low grade astrocytoma = most common brain tumor
glioblastoma multiforma (GBM) = worst brain tumor
-very aggressive and hard to treat
-lief expectancy is 11 months w treatment
Why are brain tumors resistant to treatment?
brain doesn't repair itself
is hard to determine what tissue is tumor vs. what tissue is brain during surgery
tumor cells migrate thru brain
blood brain barrier resists drug delivery
toxicity of treatments
What are risk factors of AD?
highest risk = family history AD
family history of down's
family history o fParksinons
What is AD marked by?
extracellular: beta amyloid plaques
intracellular: NFTs => neurofibrillary tangles
what is true about familial and sporadic AD?
begin differently but end the same
familiar = production
sporadic = clearance
What is regeneration?
regrowth of severed axons and reforming original synapses
can axons regenerate?
possible in PNS
never in CNS
Why is there less growth in CNS?
because neurons don't divide2
will regenerate in pns
How does "regeneration? occur in CNS?
modulatory systems => elongation occurs along blood vessels that are growing in damaged areas of the brain, but does not generate new synapse
in CNS, sprouting and modulation occurs, but no synapse
what is a chromatolytic neuron?
swelling of cell
What are possible mechanisms for partial recovery of function after brain injury?
chromatolytic (sick) neurons recover
adjustment in synaptic strength of remaining axons
learned adjustment of behvaior
What is the problem with embryonic cortex transplanted into adult host cortex in mice?
problem: foreign tissue ultimately rejected
but stem cells are the way of the future
fibrin gel promotes axon regeneration via injection of growth actor
blocking nogo factors promotes growth
What did Aguayo discover?
discovered you can fix a severed CNS axon by injecting PNS Schwann cells in this area
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