In article <4t89bj$2p3 at grieg.cs.unc.edu> Charles Schmitt,
schmitt at cs.unc.edu writes:
>pre-synaptic neuron elicits a PSP in a post-synaptic neuron with a
>given shape that, while not strictly the same over time, is fairly
>constant. By shape I'm referring to the rise-time, amplitude, decay
>time, etc... Is this correct? Also, are there mechanisms which are
Interesting question. The shape of the observed PSP results from the
combination of two categories of factors: 1) the shape of the underlying
synaptic current and 2) the properties of the cell membrane and solutions
in between the site of the synapse and your recording electrode. There is
a huge and complicated literature covering both of these aspects. Recent
papers bearing the names of David Colquhoun, Craig Jahr, Peter Jonas,
Guy Major, Bert Sakmann, Nelson Spruston and Gary Westbrook (and many
others) deal with some of these issues.
There are certainly ways to alter the shape of the synaptic current by
altering the gating characteristics of postsynaptic receptors. The
obvious examples are drugs such as general anesthetics, which prolong
GABA-A receptor-mediated IPSCs (and thus IPSPs), and cyclothiazide which
prolongs AMPA receptor-mediated EPSCs (and thus EPSPs provided the
membrane time constant is short). Other examples include endogenous
regulation of receptor kinetics by phosphorylation or whatever. A lot of
work still needs to be done in this latter area.
Another way to alter what you _think_ the PSP looks like is to change
either the membrane resistance or the series resistance between your
electrode and the synapse. For example, if the seal in a whole-cell
current-clamp recording becomes leaky, the apparent membrane time
constant will go down, and all PSPs that come from far away up a dendrite
will appear to get faster than they were in the healthy recording
situation (they'll also look a lot smaller because a lot of the injected
charge will leak out to ground instead of going through your pipette).
Another example would be if there were inhibitory synapses at the soma or
proximal dendrites, and excitatory synapses were placed distal to them
(this actually is the case for a lot of cell types). Then the inhibitory
conductances would "shunt" the excitatory PSPs, reducing both their
amplitudes and time constants as recorded at the soma. The quantitative
details of this stuff are pretty involved, I think, but see papers by
Major and Spruston for thorough treatments.
> More specifically, can a PSP which is
>normally of long duration and low amplitude be modulated by pre,post,
>or external influences into a PSP of short duration and high amplitude,
>and vice versa.
sounds like something that would happen if there were a series resistance
(or bridge balance) problem. If you have experimental data that shows
this phenomenon, you probably want to rule this option out rigorously
before pursuing a biological explanation.