Vesicular glutamate filling and AMPA receptor occupancy at the calyx of Held synapse of immature rats.

摘要: At central glutamatergic synapses, neurotransmitter often saturates postsynaptic AMPA receptors (AMPARs), thereby restricting the dynamic range of synaptic efficacy. Here, using simultaneous pre- and whole-cell recordings, at calyx Held synapse immature rats, we have investigated mechanism by which transmitter glutamate AMPARs. When loaded l-glutamate (1–100 mm) into presynaptic terminals, quantal EPSC (qEPSC) amplitude changed in a concentration-dependent manner. physiological temperature (36–37°C), qEPSC increased when intraterminal concentration was elevated from 1 mm to 10 mm, but it reached plateau mm. This persisted after bath-application low affinity AMPAR antagonist kynurenate, suggesting that caused saturation vesicular filling with rather than In contrast qEPSCs, action potential-evoked EPSCs remained unchanged increasing 100 even room temperature, indicating multi-quantal saturated could be relieved blocking desensitization cyclothiazide (100 μm). The ambient slice, estimated NMDA receptor current fluctuations, 55 nm; this far below required for desensitization. We conclude rapid desensitization, released multiple vesicles during transmission, underlies calyceal before onset hearing.