Hippocampus Ltp Ltd Etc

Front 1

what is the hippocampal formation

Back 1

buried deep within the medial temporal lobe of the human brain . consists of the dentate gyrus, hippocampus, subiculum, presubiculum, parasubiculum, and entorhinal cortex

Front 2

Hippocampus cornu ammonis

Back 2

when seen with its contralateral half resembles the coiled horns of a ram therefore named the HC cornu ammonis which now serves as acronnym for HC subfields

Front 3

LTP definition

Back 3

persistent increase in synaptic strength (as measured by the EPSP in a follower neuron) that can be induced rapidly by a brief burst of spike activity in the presynaptic afferents and this change can last for hours or even days

Front 4

First evidence of LTP

Back 4

in 1973 Bliss and Lomo demonstrated LTP in the HC of the rabbit; brief high frequency stimulation of the perforant pathway input to the dentate gyrus produced a long lasting enhancement of the extracellulary recorded field potential

Front 5

input to the hippocampus

Back 5

entorhinal cortex sends information to the HC by way of a bundle of axons called the perforant path

Front 6

perforant path axons synapse on where

Back 6

on neurons of the dentate gyrus. DG neurons give rise to axons called mossy fibers that synapse on CA3 cells

Front 7

CA3 cells

Back 7

gives rise to axons that branch one branch leaves the HC via the fornix and the other branch called the schaffer collateral forms synapses on the neurons of CA1

Front 8

LTP LTD

Back 8

candidate mechanisms for storing information in the brain, only one form can modify intrinsic electrical properties

Front 9

biopsy tissue in human

Back 9

recorded field potential

Front 10

Candidate memory storage mechanisms

Back 10

changes in synaptic function, intrinsic electrical properties, morphology, glutamate transporters

Front 11

Axon of Ca3 pyrmaidal cell and Ca1 pyrmaidal cell

Back 11

electrodes are extracellular exciting a few axons (a population) and activate separate populations of neurons. record from the soma of CA1. record a few times then give tetanic stimulation. is input specific

Front 12

tetanus

Back 12

100 hz/second

Front 13

number of CA1 synapses

Back 13

CA1 cell has about 5000 synapses

Front 14

associativity

Back 14

pair strong stimulation at pathway 1 with weak stim at pathway 2 you get LTP at pathway 2. these depend on close temporal proximity. suggest that some signal that can travel to pathway number 2

Front 15

presynaptic ways to make synapse stronger

Back 15

increase probability of NT release, increase amoutn of transmitter/vesicle
normally probability is 0.3

Front 16

postsynaptic ways to make synapse stronger

Back 16

put in more receptors at PSD, increase the unitary conductance so flux more ions/time, increased agonist affinity, change kinetics (open more quickly, close slower),

Front 17

AMPAR

Back 17

number on synapse is 0-200

Front 18

quantal analysis

Back 18

record large number of responses, sometiems they are failures

Front 19

silent synapse model

Back 19

before LTP you only have NMDAR then through maturation or LTP now you insert AMPAR

Front 20

LTD

Back 20

the inverse of LTP was first reported to occur at Schaffer collateral input to CA1 pyramidal cells

Front 21

LTD induced by

Back 21

prolonged low-frequency stimulation, bath-applied glutamate, pairing with depolarization to -40 mV so only partially relieves Mg2+

Front 22

LTD blocked by

Back 22

block with postsynaptic inhibitors of calcineurin which has a higher affinity for calcium than CaMKII

Front 23

immediate early gene

Back 23

mRNA expression is rapidly induced independent of new protein synthesis most often by new gene transcription

Front 24

GluR2 containing AMPAR

Back 24

cannot pass Ca2+

Front 25

Arc

Back 25

mRNA expression increases in cortex and HC after novel environment exploration

Front 26

Arc interacts with

Back 26

endophilin and dynamin

Front 27

overexpress Arc

Back 27

leads to decreased surface AMPAR expression due to AMPAR internalization, so Arc works to downregulate AMPAR expression to avoid over excitation

Front 28

NARP

Back 28

it is an IEG that plays a role in AMPAR clustering it is secreted from presynaptic cell to induce clustering in postsynaptic cell

Front 29

Dissociative disorders

Back 29

disruption of consciousness, identity, memory or perception of the environment and not due to medical condition or substance abuse. -dissociative amnesia, -dissociative fugue
-dissociative identity disorder, -Depersonalization disorder

Front 30

pathway important for the induction of LTP

Back 30

CaMKIIinhibitors prevents the induction of LTP

Front 31

upregulation of what receptors during LTP

Back 31

AMPA receptors are delivered to dendritic spines after repetitive stimulation accompanied by NMDA receptor activation; so you can interfere with LTP by inhibiting membrane fusion

Front 32

CaMKIIa

Back 32

can phosphorylate AMPA receptors in the membrane increasing their channel conductance and thereby increasing quantal size

Front 33

what is LTP

Back 33

a persistent increase in synaptic strength induced by brief high-frequency electrical stiulation of afferent fibers or coincident activation of pre and post synaptic neurons

Front 34

Calcium influx mediated by NMDAR

Back 34

is necessary and sufficient for the induction of E-LTP

Front 35

CaMKII and PKC

Back 35

become autonously active and able to perform phosphorylation events that underlie E-LTP expression ie. AMPA phos and PKC mediated phos of GluR1

Front 36

PKA and CaMKIV and ERK signaling

Back 36

signaling to the nucleus activates key transcription factors including cAMP-responsive element binding protein (CREB)

Front 37

one main intracellular signaling cascade activated by TrkB receptor:

Back 37

Ras-mitogen activated protein kinase MAPK pathway

Hint 37

follows recruitment and phosphorylation of Shc adaptors leads to binding of GRB2 and/or SOS and activation of Ras-MEK-ERK-RSK