抄録
Various presynaptic modulations involve changes in the presynaptic membrane potential. However, it is not entirely clear how presynaptic membrane potential determines synaptic efficacy. We addressed this issue using simultaneous pre- and postsynaptic whole-cell recordings at the calyx of Held in rat brainstem slices. Gradual decrease in the presynaptic action potential amplitude by tetrodotoxin (TTX, 20-40 nM) had no effect on the EPSCs amplitude as far as the action potential overshoot exceeded +10 mV, but further reduction below this level steeply diminished EPSCs. In the absence of TTX, presynaptic depolarization (by 10-20 mV) increased the EPSC amplitude despite a reduction in the action potential amplitude, whereas presynaptic hyperpolarization had no clear effect on EPSCs. Presynaptic Ca2+ currents, recorded after blocking sodium and potassium conductance, underwent facilitation when the nerve terminal was depolarized (15-20 mV, 2 sec). Although this magnitude of depolarization did not evoke detectable Ca2+ currents, Ca2+ measurements using fluo-4 showed a clear increase in the Ca2+ concentration in the nerve terminal. These results suggest that presynaptic depolarization increases Ca2+ influx into the nerve terminal thereby facilitating transmitter release via mechanisms involving Ca2+ -dependent facilitation of Ca2+ currents. [Jpn J Physiol 55 Suppl:S152 (2005)]
