Abstract
In the mammalian retina, rod signals from rod bipolar cells are transferred to the cone circuit via AII amcrine cells. The AII amacrine cells make sign-conserving synapses, via gap junctions, with ON-cone bipolar cells at the arboreal dendrites and glycinergic sign-inverting synapses with OFF-cone bipolar cells at the proximal dendrites. It has been reported that AII amacrine cells generate TTX-sensitive repetitive spikes of small amplitude. Using in situ hybridization, we found the expression of Nav1.1 (TTX-sensitive voltage-gated Na+ channel α-subunit) mRNA in AII amacrine cells, while the localization of Nav1.1 protein remains unclear. We found that the spike frequency increased in proportion to the concentration of puffer-applied glutamate to the arboreal dendrite and was suppressed by the puffer-applied L-AP-4, a glutamate analogue that hyperpolarizes rod bipolar cells, to the outer plexiform layer. Therefore, it is most likely that the spike frequency generated by the AII amacrine cells is dependent on the glutamatergic input from rod bipolar cells. Puffer-application of TTX to the proximal dendrite of AII amacrine cells blocked the Na+ current significantly compared with the application to other regions, indicating that the voltage-gated Na+ channels were mainly localized around the proximal dendrites. It is possible that the spikes contribute to the OFF-pathway by promoting release of glycine from the proximal dendrites in response to light intensity in scotopic vision. [J Physiol Sci. 2007;57 Suppl:S11]
