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 °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 τ 1 of 86 µs and τ 2 of 0.75 ms. At 0 °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 °C. The τ 1 of 240 µs was almost three times larger than at 10 °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.