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50 Cards in this Set

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what is the memory loop
sensory info processed at the cortex adn then transferred to association area of temporal lobe:
enterohinal, perihinal, subiculum

the info is then processed and held (consolidated) at the limbic areas (hipocampus/amygdala)

the info is then transferred back to 1 and association cortex: prefrontal, temporal, diffuse cortical areas
how do you test immediate memory?
the digit span

read some numbers and then look away and remember them.
how do you test short term meory loss
what idd you eat today
how'd you get here today
what did you wear yesterday

20 min-3 days

**interefrence is common, labile memories get distracted
in what type of memory loss is there lots of interference
short term memory

*labile memories in the recent memories of what did you eat today, what did you wear yesterday, how did yo get here?
if something is important and we want a memory what happens
we use NE/Ach in cleft to tag it as important
whats confabulation
making things up!!!

**dont think they are lying, they just want to please you with an answer

**common in short term memory loss or korsikoff pts
how do you test LONG term memory
ask abt events important to the pt!

**usually endure lots: stroke, trauma ect

**the formatio of NEW memories is hard
if you start loosing long term meory what might have happened
cortical impairemnt is getting bigger

new infarct
in learnign and memory impaird pts what type of memort are lost? what kind of info? what part of brain
explicit memory about events/facts

**hippocampus, amygdala
tell me a little about the amnesic case of HM
removed ant temporal lobe structures BL and he got a perfect anterograde amnesia, inability to learn new things

**memory before surgery intact, IQ no change, sensory and motor fx in tact
when thye removed HM's antieorr tempporal lobe what did they do to his ability to remeber new things
removed it!

Memory Loop:
1. sensory info to cortex
2. transferred to association areas of temporal lobe (enterohinal, perihinal, subliculum)
3. then the info is concolidated (processed and held) at the hippocampus and amygdala
4. the info is then sent back to primary cortex and association cortex in the prefrontal, temporal and other diffuse areas)
if i have the ability to remember things what does it mean went on in my brain?
1. i had sensory info enter by brain in the normal cortical areas

2. the info is then sent quickly to an association area os the temporal lobe (enterohinal, perihinal, subliculum)

3. then they are spun in the limbic system (hippocampus/amygdala) and consolidated here

4. then they are transferred back to the original sensory areas and you can recall all of the sensory of a memory as one interwwinded memory
int eh memory loop where is the 1 sensory info passed to?
the association cortex of temporal lobe (enterohinal, perihinal, sublenticulum)

**then its passed to limbic system (hippocampus/amygdala) where it is spun and condolidated

**after this its sent back tot eh original cortex areas and you can now remeber
what changes happen in the brain when you learn immediate, short term, long term memories
1 Immediate: activate distributed neural circuits

2. Short: synaptic efficiency, protein conformation, stimulate the limbic circuits

3. Long: new dendritic spines, axonal sprouting, RNA/protein chanves in the cortex
in general what does the L and R hippocampus do
R: cognitive spatial maps, place cells

L: words lists, language
if your L hippocampus is working what types of info is there
words, lists, language

**R is cognitive spatial maps, place cells
if ny cortex is lit up what kind of memory am i having
Immediate
if im changing protein conformation and stim limbic circuits what kind of memory
short term
if i am making new dendritic spines, having axonal sprouting and RNA/protein changes in the cortex what kind of memory am i having
long term
what hippocampus is working?

"i am facing N, the freeway is to my L and hte car is behind me"
R hippocampus

**the L is associated with language. words, lists, language
what is the thing that they think is the synaptic reason we learn
long term potentiation

**we have post synaptic R (NMDA) that make a synapse more responsive.
what is long term potention
mechanism for learning

**due to strengthened synapse after bombardment with incoming info
is LTP going on all the time'/
yep

continuous loop of hippocampus, amygdala, cortex
can you still learn if LTP is blocked
nope
whats the mech of LTP
1. sensory to hippocampus
2. presynaptic cell releases glut
3. Post synaptic cells with special glut R (NMDA) opens and lets of flood of Ca post synaptically

4. Ca leads to 2 messengers: increase post synaptic R, more presynaptic glut release, increase SA of Pre/Post

5. All strengthen the synapse nad underlie working memory
waht is NDMA Receptor? what happens as a resulf of its activation
in the post synaptic membrane in the hippocampus

**when this is bound to glutamate LOADS of Ca enter the cell and increase R, glut, and SA to make the synapse stronger!
fear and rage memories are associated with what structuer
amygdala
what memories are assoiated with fear and rage
amygdala
so LTP is what get the memories spinning in the hippocampus, what then brings the memoroes back to the cortex
REM sleep
REM sleep is important in what part of memory formation
bringing hippocampal memories back to teh cortex

**info processed really fast
so the amydgala processes memories simliar to what? whats the difference?
simlir to the hippocampus with LTP: NADM receptors influc of Ca--> increased glut, increased R, increased SA

**the only differnece is amydgala is fear memories and hippocampus is all other memories
what can the amydgagla do when it processes its fear memories
activate SNS for fear response
does the amydgala or hippocampus have benzodiazepene R
amygdala

**valume shuts off this fear response associated with teh amygdala
when is hte first memory
3 or 4 when hippocampus forms

**the amygdala develops a bit earlier so can have earlier negative memories
what happens with a temporal lobe leision? whats the syndrome
kluver Bucy syndrome

**sexual!
**hyperattentive
**placid (cant be excited)
**cant recognize things visually (agnosia) so are hyper oral
what is Kluver Bucy syndrome, what does it look like, where is the leision
hyper sexual, placid, hyperattentive, cant recognize things visually so you try orally

**temporal lobe leision
what neuromodulator is associated with...

1. attention
2. arousal
3. inhibitory transmission
Ach
NE
GABA
GABA is associated with what? what about NE and Ach
Ach: attention
NE: arousal
GABA: inhibitory transmission
whate are cholinergic agonists
acetylocholineesterase inhibitors, keeps mroe Ach around

Ex: physostigimine
Tacrine
Aricept
Exelon
what NT is initially affected in AD
Ach
what part of the forebrain is cholinergic, what does this do
basal forebrain, attention
septum: into hippocampus directly, memory
what cells are initially killed in AD?
cholinergic cells that go to the basal foerbrain and septum (to hippocampus)
can we increase NE system to increase memory?
nope

NE is for arousal, ie caffeine, amphetamines, NE, epinepherine
where is NE made, what does it do
locus coeruleus

**arousal, wont increase memory
what is an amnestic agent
GABA agonists (sedative/hypnotics: benso, barbituates, EtOH, versed)

Cholinergic Antoginist
B blockers
**these last 2 are not so much
what do GABA agonists do to learning/memory
inhibit it! amnestic effects
other that GABA agonists what are the more mild forms of amnestic agents
cholinergic antagonists
B blockers
what is goind on it AD (alzheimers disease)
thrple whammy
loss of:
1. hippocampus
2. The chilinergic inputs into teh hippocampus via septum
3. The sensory inputs

**all are lost so its a fx isolation of the hippocampus
in what disease do we see a fx isolation of the hippocampus
AD

loose fx of
1. hippocampus itself
2. cholinergic input from septum into the hippocampus
3. the sensory input to the hippocampus
what is the way we are tx AD currently?
1. cholinesterase inhibitors
2. Prevention: LEARN, use it or loose it