抄録
AII amacrine cells (AIIs) play a crucial role in the rod pathway of the mammalian retina: they receive glutamatergic input from rod bipolar cells (RBCs), and also send sign-conserving output at distal dendrites via gap junctions and glycinergic sign-inverting output at proximal dendrites. AIIs generate TTX-sensitive spikes. To investigate functional role of the spike, we performed whole-cell patch clamping of AIIs in the mouse retinal slice preparation. Local application of glutamate to the dendrites of AIIs increased spike frequency in dose-dependent manner. When depolarizing current was injected, repetitive spikes were evoked. Frequency of the spike was dependent on intensity of the injected current. Normalized spike frequency was plotted against the mean membrane potential (MMP) for both glutamate application and current injection experiments. Data were fitted with Boltzmann function to estimate Vf1/2 (MMP at which spike frequency was the half-maximum). Vf1/2 for current injection was similar to that for local application of glutamate to the dendrites (about -50 mV). Thus, it is likely that spike frequency of AII is dependent on excitatory glutamatergic input from RBCs. To examine the localization of voltage-gated Na+ channels (Navs) within AII, 1 μM TTX was applied. Application of TTX to the proximal dendrite and the soma blocked Na+ current more effectively than that to the distal dendrite, indicating that Navs mainly localize around the soma. Localization of Navs at the soma and the proximal dendrites may be important for effective release of glycine in signal processing. [Jpn J Physiol 55 Suppl:S169 (2005)]
