In slices from the visual cortex of kittens maintained in vitro, long-
term potentiation of synaptic transmission following high frequency st
imuli (10 Hz, 2 min) delivered at low to medium stimulus intensities (
80 to 200 mu A), is accompanied by changes of certain electrophysiolog
ical measures recorded intracellularly, such as long-lasting depolariz
ation of membrane potential and decreased threshold to elicitation of
an action potential. These parameters have never before been shown to
be altered following high frequency stimulation in other systems widel
y used in studying synaptic plasticity, such as in hippocampal neurons
. Another important difference between results from these two systems
is that the amplitude of the excitatory post-synaptic potential is enh
anced after high frequency stimulation in hippocampal neurons, whereas
in striate cortex from young kittens, we observed a decrease. We demo
nstrate here that this decrease can be reversed to show enhancement fr
om the original amplitude, upon clamp of membrane potential back to th
e voltage observed prior to stimulation. Thus, what appears to be ''lo
ng-term depression'' of synaptic transmission, as recorded extracellul
arly and represented by diminished flow of synaptic current, can be re
versed by stepping membrane voltage back to the pre-high frequency sti
mulation level, to produce responses that then become consistent with
long-term potentiation.