Glutamatergic autoinhibition of quantal release augments the early phase of releases after a depolarization pulse.
At the crayfish neuromuscular junction, glutamatergic autoinhibition of quantal excitatory postsynaptic current (qEPSC) release is mediated by a presynaptic DL-glutamate transporter and its associated Cl- conductance. I investigated whether it also affects the time course of release. qEPSCs were recorded with a perfused macroelectrode through which depolarization pulses and D- or L-glutamate could be applied to a terminal. In order to represent the time course of release, cumulative delays of qEPSCs were determined and scaled to a common final value. At 10 degrees C, on the application of D- or L-glutamate, release increased relative to the controls especially during its first millisecond, taking the mean of 20 experiments (P< 0.01). Also, in many single experiments the respective shifts in the time courses of release were highly significant. The relative surplus of early releases decreased with time constants tau1 of 86 micros and tau2 of 0.75 ms. At 0 degrees C, in the presence of glutamate, the surplus of early delays was increased relative to the controls to a significantly greater extent and for a longer time than at 10 degrees C. The tau1 of 240 micros was almost three times larger than at 10 degrees C. Autoinhibition was inactivated in Cl(-)-free solution. In such solutions the surplus of early releases also disappeared and the shortening of early delays reverted to a lengthening. Interaction of the inhibitory autoreceptor and its associated Cl- flow with the release machinery is discussed.