抄録
We addressed the mechanism ofsynaptic modulations induced by changes in the presynaptic membrane potential, using simultaneous pre- and postsynaptic whole-cell recordings at the calyx of Held in rat brainstem slices. A weak sustained depolarization (from -70 mV to -60 mV) of calyceal presynaptic terminal increased the EPSC amplitude despite that it diminished presynaptic action potential amplitude. However, as we further depolarized the terminal (to -50 mV), the amplitude of EPSC become eventually depressed concomitantly with a marked reduction in the presynaptic action potential amplitude. When the presynaptic action potential amplitude was gradually decreased by tetrodotoxin (TTX, 20-40 nM), the EPSCs amplitude remained the same as far as the action potential overshoot exceeded +10 mV, but upon further reduction of the overshoot EPSCs steeply diminished. When presynaptic Ca2+ currents (IpCa), induced by an a.p.- waveform command pulse that is recorded from calyceal terminal, were used to evoke EPSCs, a weak sustained depolarization (15-20 mV, 1 sec) enhanced both IpCa and EPSCs in parallel. 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. We conclude that weak prolonged presynaptic depolarization increases Ca2+ into the nerve terminal, and the P/Q-type specific Ca2+ induced channel facilitation plays an essential role in the facilitation of transmitter release following presynaptic depolarization. [J Physiol Sci. 2008;58 Suppl:S122]
