Abstract
AII amacrine cells play an important role in the rod pathway of the mammalian retina, extending bistratified dendrites into the inner plexiform layer (IPL). Recent studies of electrophysiological analysis of AII amacrine cells demonstrated that TTX-sensitive small spikes (10-15 mV in amplitude) were activated at low threshold (~ -55 mV), but the detail is unclear. To investigate functional role of the spike in signal processing, we examined AII amacrine cells in the mouse retinal slice, using whole-cell patch-clamp recording. Spontaneous spike generation of AII amacrine cell was suppressed by puff application of glutamate, the transmitter of the rods, to the OPL where rods and rod bipolar cells (RBCs) make synapses. It is likely that glutamate hyperpolarized the RBC, which is presynaptic to the AII amacrine cell, and decreased its glutamate release. When depolarizing current was injected at a holding potential of -70 mV, repepetive spikes were evoked. Frequency of the spike was dependent on intensity of the injected current. Moreover, puff application of glutamate to the dendrites of AII amacrine cell in the IPL made spike frequency increase in proportion to the concentration of glutamate. To examine the localization of voltage-dependent Na+ channels, TTX was applied to the various region of the dendrite and soma of AII amacrine cell. Application of 1 μM TTX to proximal dendrite and/or soma blocked Na+ current much effectively than to distal dendrite. Our results indicate that the intensity of glutamate input from RBCs may be coded by frequency of the spikes around the soma of AII amacrine cell. [Jpn J Physiol 54 Suppl:S163 (2004)]
