Michael D. Miyamoto, Ph.D.
My research focuses on how repetitive
stimulation increases transmitter release from motor nerves
during the post-stimulation period. This enhancement of
synaptic transmission or “facilitation” (lasting
several minutes) is a type of short-term plasticity that may
shed light on phenomena such as learning and memory.
Facilitation is believed to be due to the buildup of ionic
calcium (required for exocytosis) in the nerve terminal that
results from entry through membrane channels. The decay in
facilitation is presumably due to sequestration and extrusion
of the ionic calcium by various processes. The time course of
decay can be separated into four distinct components, which
suggests that at least four processes (organelles?) play a
role in terminating facilitation. The experimental approach
involves the use of electrophysiology to monitor quantized
(vesicular) transmitter release at single synapses. Its
primary advantage is to allow investigation of the dynamics
of facilitation and its decay, in intact nerve terminals on a
“real-time” basis (millisecond time scale).
Statistical patterns of quantal transmitter release and a
mathematical model of the release process are used to
dissociate the effects of various physiologic and
pharmacologic manipulations on the four components of decay.
Conceivably, modification of the decay process by certain
agents may be a way to selectively prolong facilitation,
which may be helpful in treating disorders involving
deficiencies in synaptic transmission.