抄録
Transient rise of Ca2+ at presynaptic nerve terminals triggers transmitter release. Amplitude, kinetics and distribution of Ca2+ transient within the nerve terminal regulate release modality. At the calyx of Held, the giant presynaptic terminal in auditory brainstem, injection of EGTA into the terminal attenuated EPSC amplitude at postnatal day (P)7. This effect of EGTA was diminished at P14, suggesting that Ca domain size shrinks during development. However characteristics of Ca2+ transient within the nerve terminal are poorly understood and its developmental profile remains elusive. To investigate these issues, we tried imaging for a single action potential-evoked Ca2+ transient using a low affinity Ca2+ indicator Oregon Green BAPTA/5N. Confocal spot measurement enabled detection of Ca2+ gradients within the terminal. Ca2+ transients were mainly observed at the synaptic site of the terminal, but the spatial distribution was sparser in older animals (P13-14 vs. P7-P8). Amplitude of the transient was smaller in older animals. In contrast, the rise time was determined by action potential duration, and decay time was regulated by Ca2+ buffer concentration at the both age groups in similar manner. At P7 reducing functional Ca2+ channel number by applying ω-AgTX diminished the effect of EGTA injection on EPSC. These results indicate that decrease in Ca2+ channel density contributes to developmental shrinkage of Ca2+ domain size at this nerve terminal. [J Physiol Sci. 2008;58 Suppl:S121]
