Class Notes (1,100,000)
CA (620,000)
UTSG (50,000)
CSB (500)
Lecture 11

CSB332H1 Lecture Notes - Lecture 11: Synaptic Plasticity, Chemical Synapse, Electrical Synapse


Department
Cell and Systems Biology
Course Code
CSB332H1
Professor
Melanie Woodin
Lecture
11

This preview shows half of the first page. to view the full 3 pages of the document.
CSB332H1S L11; Feb. 15, 2012
Synaptic Plasticity
Read Ch. 16
Plasticity is the capacity of the nervous system to change
Today talking about short-term
Synaptic plasticity = the capacity to alter the strength of synaptic
transmission
o Modifying connections
o Short-term (ms - mins, don’t normally require prot synthesis) or
long-term (hrs, need prots to maintain long-term, GABA)
o Can be due to Presynaptic &/or Postsynaptic changes
Most short-term due to Presynaptic
Most long-term need Postsynaptic (need retrograde
signalling)
Always changes on both sides of synapse
o = a change in synaptic efficacy or strength
Efficiency of transmission
Hebbian (Activity-dependent)
o Talking about most
o Plasticity induced by pattern of electrical activity (act pot firing)
o Hebb = name of famous Canadian neuropsychologist
or Heterosynaptic (Activity-independent)
o chemical LTP, using some kind of ligand, without changing
pattern of act pot firing
How can we test for synaptic plasticity?
Mostly looking at neuromuscular junction
To test strength of synapse:
o Stimulating electrode placed in presynaptic cell or bundle of
axons & Recording electrode placed in postsynaptic cell or
muscle
Stimulation of presynaptic cell firing of a presynaptic AP & release
of neurotransmitter
Binding of neurotransmitter postsynaptically opens ion channels
(ionotropic or metabotropic) synaptic pot recorded
postsynaptically
Amplitude of synaptic pot recorded postsynaptically is a measure of
strength of synapse
o Using test pulse/stimulation first
o First use low freq (Hz) to stimulate 1 act pot (don’t usually
activate synapse or induce plasticity on own)
1 Hz = 1 stimulation per second (1 act pot)
o Test for 10min to make sure have steady baseline
Initial baseline-recording period
o Once confident in baseline, induce plasticity (Induction
Protocol)
Then test synapse again like in baseline test, see if changed
strength (amplitude changes), compare to baseline
See if change persists after induction
Stimulating electrode in bundle of presynaptic axons in hippocampus
Recording electrode on dendrites in CA1 region
Synaptic Plasticity
Arrival of indiv APs presynaptically don’t usually activate synapse
Trains of APs are more common
Such ongoing activity can have significant effects of strength of
synapse
Changes in synapse strength = changes in synaptic efficacy
When activity (trains or patterns of APs) cause change in synaptic
efficacy:
o Activity-dependent synaptic plasticity
Key w synaptic plasticity:
o Change in synapse strength persists after activity (ex. train of
APs) that induced plasticity
Changes in presynaptic &/or postsynaptic [Ca2+]i underlie most
forms of synaptic plasticity
o ex. phosphorylates AMPA recs
Mechanisms often classified as presynaptic or postsynaptic
Long-term potentiation = most-studied form of synaptic plasticity
Short-term
Looking at amplitudes in postsynaptic muscle
Can induce two types of plasticity at same synapse
Mech is Ca
In general, most synapses are more likely to either be facilitated or
depressed
Stimulate 4 times produces 4 end-plate pots of dif sizes
o increase = facilitation
o Wait a couple ms stimulation second end-plate pot = larger
than initially was, but not as large as biggest
Artificially regulating level of extracellular Ca
o Short term mechs are dependent on amt of Ca, so trying to
exaggerate to illustrate pt
Bathed tissue in lower level of extracellular Ca
o mech underlying facilitation partially due to amt of Ca in
presynaptic synaptic terminal
Time for chelation & for levels to rise again
Ca levels normally build more neurotransmitter
released
So 3ms later, end-plate pot larger
But 1 sec later, response gone
o At NMJ, firing 1 act pot can often cause a postsynaptic act pot,
but want to measure underlying end-plate pots end-plate
pots smaller
Effect outlasts initial induction stimulus but lasts shortly for only a
second
B: bath synapse in high level of Ca
o Also puts curare in bath (antagonist of Ach) lowers synaptic
response
o Mech depends on amt of Ca
o depression
o Release a lot of quanta but subsequent atc pots are smaller
Ca comes in, nearly all vesicles released so that less
available to be released at 2nd act pot
Rapidly depleted synaptic vesicles
You're Reading a Preview

Unlock to view full version