How sodium and calcium ion channel help to visual in eyes?
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B3H 4H7 output synapse and may transduce NO signals from other cells by either directly permitting Ca2+ influx or by providing depolarizing influences that gate voltage-dependent Ca2+ channels.
Presynaptic Ca2+ channels mediate early stages of visual information processing in photoreceptors by facilitating the release of neurotransmitter and by receiving modulatory input that alters transmission. Two types of L-type Ca2+ channels, composed of α1F and α1D subunits and having similar biophysical and pharmacological properties, appear to form the principle voltage-dependent Ca2+ influx pathways in rods and cones, respectively. The role played by these channels in neurotransmitter release at these graded potential, nonspiking synapses, has been well described. The channels mediate sustained glutamate release in darkness where the cells rest at potentials near 40 mV, and signal increases in light intensity as the cells hyperpolarize negative to this value. Synaptic modulation and integration mediated by these channels has not yet been as fully described but appears to involve GABA, nitric oxide (NO), glutamate, and dopamine. Ca2+ permeable, cyclic nucleotide-gated (CNG) channels appear to have supporting roles at the photoreceptor.