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Lecture 15

CSB332H1 Lecture Notes - Lecture 15: Synaptic Plasticity, Schaffer Collateral, Biological Neural Network

Cell and Systems Biology
Course Code
Melanie Woodin

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CSB332H1S L15; March. 12, 2012
Inhibitory Synaptic Plasticity in the Hippocampus
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Interviewing patient EP lost hippocampi selectively due to a virus
o Also tissue immediately around it
Interviewed almost weekly since
Deep in temporal lobe, so hard to remove without damaging other
Also no neurogenenerative disease that results in only this loss
EP now 82; acute virus in 1992, more thinking skills virtually intact
o Can copy complex drawings, read back list of words, amazed at
o Repeats self often & unaware (was in electronics, computers
used to fill a room)
o Enjoys the expts, unsure if met expt’ers before, can’t remember
names even though visited over 200 times
o Has a record of the experiences been positive, lets expt’ers in
door faster, built repor’ w expt’ers
o Can’t rmbr 15mins ago
o Can remember childhood vividly (ex. how to get places,
remembering streets & directions, maps)
So hippocampus can’t be where memories permanently
stored, but crucial for recording new memories
But does not know streets where he currently lives
Hippocampus required to store long-term memories
LTP = model of cellular basis of memory
Synaptic plasticity occurs at both excitatory & inhibitory synapses
Classic excitatory glutamatergic long-term potentiation has been well
characterized in numerous systems
Inhibitory synaptic plasticity has been less well-characterized despite
its known roles in regulating neuronal network activity
Long-Term Objectives of the Woodin Lab
To determine how electrical &physiological activity in the brain
modifies inhibitory synapses (termed inhibitory synaptic plasticity)
What are the mechanisms underlying inhibitory synaptic plasticity
To understand how inhibitory synaptic plasticity contributes to:
o the cellular basis of learning & memory, and
o information processing in the brain
fn’al significance of inhibition in laying down memories
GABAA Receptor
Ligand-gated ion channel
Largely permeable to Cl-
Contains numerous binding sites for allosteric modulators
GABA not always inhibitory but main inhibitory in adult CNS
Glycine also inhibitory but more often found in spinal cord, rec similar
3 types, A & B most common
A = ionotropic, mostly permeable to Cl, also permeable to bicarbonate
o Many endogenous binding sties for allosteric modulators
Barbiturates, steroids
B = metabotropic signal cascade open K channels
What determines the strength of inhibitory synapses?
Synaptic conductance depends on:
o amt of transmitter release
o # & conductance of postsynaptic transmitter recs (GABA A)
Driving force for Cl-
o Specific for GABA A
o If levels rise reverses pot of GABA above resting pot, so
In all organisms examined to date, have developmental changes in
levels of Cl esp in first 2 weeks after birth (postnatal development,
goes lower)
o In pathological disorders (ex. schizophrenia) Cl higher
o No evidence that other ion grads affect these
driving force
(EGPSC or ECl)
We determine the strength of GABAA-mediated synaptic transmission
by measuring the reversal pot for GABA (EGABA); EGABA is the value of
the membrane pot where there is no net flow of Cl- ions thru the
Balena & Woodin 2008 European Journal of Neuroscience
What changes in reversal pot for GABA determined by level of Cl
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