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Voltage-dependent sodium channels are expressed in nonspiking retinal bipolar neurons.

ABSTRACT: Retinal bipolar neurons transmit visual information by means of graded synaptic potentials that spread to the synaptic terminal without sodium-dependent action potentials. Although action potentials are not involved, voltage-dependent sodium channels may enhance subthreshold depolarizing potentials in the dendrites and soma of bipolar cells, as they do in other CNS neurons. We report here that voltage-dependent sodium currents are observed in a subset of bipolar neurons from goldfish retina. Single-cell reverse transcriptase-PCR identified four different sodium channel alpha subunits in goldfish bipolar cells, putatively corresponding to the mammalian voltage-gated sodium channels Na(v)1.1, Na(v)1.2, Na(v)1.3, and Na(v)1.6. The amount of sodium current was largest in cells with smaller synaptic terminals, which probably represent cone bipolar cells. Localization of sodium channel immunoreactivity in goldfish retina confirmed the expression of voltage-gated sodium channels in cone bipolar cells of both ON and OFF types. Both immunocytochemical and physiological evidence suggests that the sodium channels are localized to the soma and dendrites where they may play a role in transmission of synaptic signals, particularly in the long, thin dendrites of cone bipolar cells.

SUBMITTER: Zenisek D

PROVIDER: S-EPMC6762356 | biostudies-literature | 2001 Jul

REPOSITORIES: biostudies-literature

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Voltage-dependent sodium channels are expressed in nonspiking retinal bipolar neurons.

Zenisek D D Henry D D Studholme K K Yazulla S S Matthews G G

The Journal of neuroscience : the official journal of the Society for Neuroscience 20010701 13

Retinal bipolar neurons transmit visual information by means of graded synaptic potentials that spread to the synaptic terminal without sodium-dependent action potentials. Although action potentials are not involved, voltage-dependent sodium channels may enhance subthreshold depolarizing potentials in the dendrites and soma of bipolar cells, as they do in other CNS neurons. We report here that voltage-dependent sodium currents are observed in a subset of bipolar neurons from goldfish retina. Sin ...[more]

PMID: 11425883

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Project description:Voltage-dependent Na+ channel activation underlies action potential generation fundamental to cellular excitability. In skeletal and cardiac muscle this triggers contraction via ryanodine-receptor (RyR)-mediated sarcoplasmic reticular (SR) Ca2+ release. We here review potential feedback actions of intracellular [Ca2+] ([Ca2+]i) on Na+ channel activity, surveying their structural, genetic and cellular and functional implications, translating these to their possible clinical importance. In addition to phosphorylation sites, both Nav1.4 and Nav1.5 possess potentially regulatory binding sites for Ca2+ and/or the Ca2+-sensor calmodulin in their inactivating III-IV linker and C-terminal domains (CTD), where mutations are associated with a range of skeletal and cardiac muscle diseases. We summarize in vitro cell-attached patch clamp studies reporting correspondingly diverse, direct and indirect, Ca2+ effects upon maximal Nav1.4 and Nav1.5 currents (Imax) and their half-maximal voltages (V1/2) characterizing channel gating, in cellular expression systems and isolated myocytes. Interventions increasing cytoplasmic [Ca2+]i down-regulated Imax leaving V1/2 constant in native loose patch clamped, wild-type murine skeletal and cardiac myocytes. They correspondingly reduced action potential upstroke rates and conduction velocities, causing pro-arrhythmic effects in intact perfused hearts. Genetically modified murine RyR2-P2328S hearts modelling catecholaminergic polymorphic ventricular tachycardia (CPVT), recapitulated clinical ventricular and atrial pro-arrhythmic phenotypes following catecholaminergic challenge. These accompanied reductions in action potential conduction velocities. The latter were reversed by flecainide at RyR-blocking concentrations specifically in RyR2-P2328S as opposed to wild-type hearts, suggesting a basis for its recent therapeutic application in CPVT. We finally explore the relevance of these mechanisms in further genetic paradigms for commoner metabolic and structural cardiac disease.

Dataset Information

Voltage-dependent sodium channels are expressed in nonspiking retinal bipolar neurons.

Publications

Voltage-dependent sodium channels are expressed in nonspiking retinal bipolar neurons.

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