抄録
Among glutamatergic synapses, contribution of AMPA receptor (AMPAR) desensitization to short-term synaptic depression is variable. We addressed the mechanism by which AMPAR desensitization is involved in synaptic depression at the calyx of Held synapse of developing rats. AMPA-EPSCs showed a strong paired-pulse depression (PPD) at postnatal day (P) 7, but PPD became weaker as rats matured. The recovery time from AMPAR desensitization, assessed by paired-pulse glutamate applications to outside-out patches from postsynaptic neurons, became shorter with development. Cyclothiazide (CTZ), which completely blocked AMPAR desensitization, attenuated PPD at P7, but not later than P14, suggesting that AMPAR desensitization contributes to synaptic depression only at immature synapses before the hearing onset (P10). Matching Pr at P14 synapses to that at P7, by increasing external Ca2+ and adding tetraethylammonium, recruited a CTZ-sensitive component in PPD. Quantitative single-cell RT-PCR analyses indicated that the R/G-edited GluRs increase with development, and that the recovery AMPARs from desensitization was faster in patches from cells having R/G-edited GluRs more abundantly. We conclude that a developmental decrease in Pr, together with a developmental increase in the R/G-edited GluRs, reduces contribution of AMPAR desensitization to synaptic depression. [J Physiol Sci. 2007;57 Suppl:S19]
