抄録
AMPA receptors (AMPARs) mediate fast synaptic transmission at the calyx of Held. At the postnatal day 7 (P7) EPSCs are characterized with slow decay time and strong paired-pulse depression (PPD), but the decay time becomes faster and the magnitude of PPD decreases as animals mature. Using fast glutamate application to outside-out patches excised from postsynaptic MNTB neurons, we examined whether the desensitization and deactivation of postsynaptic AMPARs might contribute to these developmental changes. Throughout development (P6-21) the decay time constant of miniature (m) EPSCs was similar to that of AMPAR deactivation. Cyclothiazide (CTZ) almost abolished AMPAR desensitization, and prolonged AMPAR deactivation. CTZ also prolonged mEPSC decay time, with the magnitude of prolongation being inexplicable simply by that of AMPAR deactivation, particularly at the early postnatal period. CTZ also abolished PPD of glutamate-induced AMPAR currents, and reduced the magnitude of synaptic PPD at P7, but not after P14. In the single cell RT-PCR analysis the abundance of GluR4 flop subunit showed a positive correlation with the mEPSC decay time at P7, but not after P14. We conclude that postsynaptic AMPAR desensitization contributes to the decay time of EPSCs and synaptic depression at the early period, but its contributions become less as animals mature. [Jpn J Physiol 54 Suppl:S139 (2004)]
