Lecture 11

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Department
Cell and Systems Biology
Course
CSB332H1
Professor
Melanie Woodin
Semester
Winter

Description
CSB332H1S L11; Feb. 15, 2012  Key w synaptic plasticity: Synaptic Plasticity o Change in synapse strength persists after activity (ex. train of Read Ch. 16 APs) that induced plasticity  Changes in presynaptic &/or postsynaptic [Ca2+]i underlie most Plasticity is the capacity of the nervous system to change forms of synaptic plasticity  Today talking about short-term o  ex. phosphorylates AMPA recs  Synaptic plasticity = the capacity to alter the strength of synaptic  Mechanisms often classified as presynaptic or postsynaptic transmission  Long-term potentiation = most-studied form of synaptic plasticity 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  Short-term  Looking at amplitudes in postsynaptic muscle strength of synapse  Can induce two types of plasticity at same synapse o Using test pulse/stimulation first  Mech is Ca o First use low freq (Hz) to stimulate 1 act pot (don’t usually activate synapse or induce plasticity on own)  In general, most synapses are more likely to either be facilitated or  1 Hz = 1 stimulation per second (1 act pot) depressed o Test for 10min to make sure have steady baseline  Stimulate 4 times  produces 4 end-plate pots of dif sizes o  increase = facilitation  Initial baseline-recording period o Wait a couple ms  stimulation  second end-plate pot = larger o Once confident in baseline, induce plasticity (Induction Protocol) than initially was, but not as large as biggest  Then test synapse again like in baseline test, see if changed Artificially regulating level of extracellular Ca strength (amplitude changes), compare to baseline o Short term mechs are dependent on amt of Ca, so trying to  See if change persists after induction 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,  Stimulating electrode in bundle of presynaptic axons in hippocampus but want to measure underlying end-plate pots  end-plate pots smaller  Recording electrode on dendrites in CA1 region  Effect outlasts initial induction stimulus but lasts shortly for only a Synaptic Plasticity second  Arrival of indiv APs presynaptically don’t usually activate synapse  B: bath synapse in high level of Ca  Trains of APs are more common o Also puts curare in bath (antagonist of Ach)  lowers synaptic response  Such ongoing activity can have significant effects of strength of o Mech depends on amt of Ca synapse o  depression  Changes in synapse strength = changes in synaptic efficacy  When activity (trains or patterns of APs) cause change in synaptic o Release a lot of quanta but subsequent atc pots are smaller efficacy:  Ca comes in, nearly all vesicles released so that less available to be released at 2 act pot o Activity-dependent synaptic plasticity  Rapidly depleted synaptic vesicles o If were to stimulate again, would see end-plate pot at 300ms o Hard to measure underlying amplitude of end-plate pots, want would still be smaller (outlasts stimulus), but back to normal to weaken by hyperpolarizing membrane pot so at more after 1 sec (enough time to move vesicles from reserve pool to negative value further from threshold  more unlikely to reach terminal) for act pot o Ca levels usually constant in cerebrospinal fluid o Stimulate synapse  record wave form w two parts  Depends on microdomains & other factors regulating  Initial peak than secondary peak neurotransmitter release  Initial peak doesn’t change in amplitude  C: combine A & B  Indicates there is an electrical synapse, not chemical; o Get some elements of fac & depr occurring together also know since see response immediately o Get fac but then 3 & 4 are same  Secondary wave form = end-plate pot o At 300ms, test synapse, response much smaller so synapse has o Test strength of synapse (control) undergone a depression o Induction protocol  then see if plasticity occurs  So need to test synapse after the Induction Protocol and  T=0 compare to initial test  Don’t care what it looks like during induction o 15s after, test strength  huge end-plate pot that leads to act pot; so know there has been huge increase in synapse strength; end-plate pot was 1mV before o Wait 1min, test again  see huge end-plate pot but not enough to reach threshold o By 10min, returns close to baseline but still larger, so know isn’t long-term form of
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