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Printable Handouts
Navigable Slide Index
- Introduction
- Synaptic plasticity to natural spike trains
- Synaptic depression and enhancement
- Synaptic plasticity can be target-dependent
- Synaptic transmission is quantized
- Variance analysis
- Part I: synaptic depression
- Depression in a train
- The simple depletion model
- Properties of depression fit the model
- Depletion S and F are not binomial n and p
- Fast depression can be multi-component
- Slow phases of depression
- Evidence for distinct vesicle pools
- Unloading the RRP causes fast depression
- Evidence for distinct vesicle pools
- Recovery of the RRP is mainly from the RP
- Calcium-dependent mobilization
- Some synapses don’t depress at all
- Other forms of synaptic depression
- Less common forms
- Part II: synaptic enhancement
- Facilitation often has two components
- Facilitation may summate linearly
- The linear summation model is imperfect
- PTP, a slower phase
- Augmentation in intermediate phase
- Facilitation to constant depolarizations
- The role of calcium
- Decay of [Ca2+]i and facilitation
- Decay of [Ca2+]i and augmentation
- Mitochondria and PTP
- Post-tetanic mPSP frequency
- [Ca2+]i reduction rapidly reduces facilitation…
- …and reduces augmentation/PTP, but with a delay
- Problems with the single site hypothesis
- Inconclusive suggestions of Ca2+ action sites
- The search for molecular mediators
- Synapsin, CaMKII, and PTP
- Munc18, PKC, and in PTP
- Myosin, MLCK, and PTP
- Munc13-2, calmodulin, and augmentation
- PKA in facilitation and PTP
- rab3, and rim in facilitation
- Facilitation by buffer saturation
- NCS-1 and other players in facilitation and PTP
- Putting it all together
- Less common forms of enhancement
- Part III: functional roles
- Network modeling
- Real physiological examples
- Conclusion & acknowledgments
Topics Covered
- What is short-term synaptic plasticity?
- Use of quantal analysis to show that plasticity arises presynaptically
- Synaptic depression and the "Depletion Model"
- Relationship of depletion model parameters to binomial statistical parameters
- Refinements to the depletion hypothesis
- Origin of slow phases of depression
- Role of multiple vesicle pools
- Role of vesicle endocytosis
- Role for calcium in recovery
- Why depression is sometimes absent
- Other forms of depression
- Phases of synaptic enhancement: facilitation, augmentation, and potentiation
- Presynaptic electrical events in synaptic enhancement
- Calcium and the nonlinear summation single site hypothesis
- Kinetic components of calcium removal
- Multiple sites of calcium action
- Problems with identifying molecular mediators
- Candidate molecular mediators
- A comprehensive model of presynaptic plasticity
- Other forms of synaptic enhancement
- Computational roles of short-term synaptic plasticity
- Physiological roles of short-term synaptic plasticity
Links
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Talk Citation
Zucker, R.S. (2014, April 9). Presynaptic plasticity [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved November 23, 2024, from https://doi.org/10.69645/QZOX6140.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Robert S. Zucker has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
A selection of talks on Neurology
Transcript
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0:00
Hello.
My name is Bob Zucker.
And I'm at the University
of California Berkeley.
You have selected a Henry Stewart
Talk on presynaptic plasticity.
0:13
Neurons rarely fire single
isolated action potentials.
They signal information with
trains of spikes that could be more
or less regular, irregular,
bursty, or sparse.
When these action potentials
invade nerve terminals,
they evoke transmitter release at
synapses, exciting or inhibiting
neighboring cells to communicate
and process information.
Synapses transmit signals of
this activity in complex ways.
The postsynaptic potentials they
generate are rarely constant.
They may wax or wane or both
compared to their amplitudes
to infrequent presynaptic
action potentials.
At vertebrates central
synapses, the slide
shows the effects of a natural
pattern of presynaptic spikes
on the top rows, evoking a mixture
of facilitated and depressed PSPs,
shown in the graph.
Responses are often complicated.
They can grow, then
decline, and then
sometimes even grow
again during a burst.
And afterwards, they can be larger
or smaller than isolated responses.
When changes in synaptic efficacy
occur in a timeframe of seconds
or, at most, a few
minutes, the changes
are classified as short-term
synaptic plasticity.
The underlying mechanisms
and physiological roles
are distinct from longer
lasting changes in transmission
lasting hours or days
and referred to as
long-term potentiation
or depression.
These are discussed in a
separate Henry Stewart Talk,
while here I will consider only
short-term synaptic plasticity.