Nitric oxide promotes GABA release by activating a voltage-independent Ca2+ influx pathway in retinal amacrine cells

摘要: Retinal amacrine cells express nitric oxide (NO) synthase and produce NO, making NO available to regulate the function of cells. Here we test hypothesis that can alter GABAergic synaptic output We investigate this using whole cell voltage clamp recordings Ca2+ imaging cultured chick retinal When recording from receiving input other cells, find increases spontaneous postsynaptic current (sPSC) frequency. This increase in sPSC frequency does not require canonical receptor, soluble guanylate cyclase, or presynaptic action potentials. However, removal extracellular buffering cytosolic both inhibit response NO. In experiments, confirm processes by activating a influx pathway. Neither nor elevations are dependent upon release stores. also enhances evoked responses. Because voltage-gated channel is altered increased likely due combined effect voltage-dependent adding NO-dependent, voltage-independent, influx. Insight into identity pathway provided transient receptor potential (TRPC) inhibitor clemizole, which prevents NO-dependent elevations. These data suggest production inner retina will enhance Ca2+-dependent GABA TRPC channel(s).NEW & NOTEWORTHY Our research provides evidence promotes canonical-mediated mechanism promoting be independent, suggesting that, retina, local bypass formal circuitry inhibition.