Sodium channel internalization in developing neurons.

B Dargent; C Paillart; E Carlier; G Alcaraz; M F Martin-Eauclaire; F Couraud

doi:10.1016/0896-6273(94)90035-3

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Sodium channel internalization in developing neurons.

B Dargent·C Paillart·E Carlier·G Alcaraz·M F Martin-Eauclaire·F Couraud

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Abstract

Neurotoxin-induced activation of voltage-dependent Na+ channels provoked rapid (t1/2 = 15-20 min) channel down-regulation in cultured rat brain neurons, resulting in a 50%-70% decrease in [3H]saxitoxin and 125I-alpha-scorpion toxin binding capacities as well as a decrease in Na+ peak current. Experiments using 125I-alpha-scorpion toxin as both a Na+ channel activator and a surface channel probe showed that a fraction of the bound toxin was internalized, since it was not releasable by acidic washing. Internalization was inhibited by tetrodotoxin, abolished in Na(+)-free medium, and induced by amphotericin B, a Na+ ionophore. Moreover, down-regulation occurred only in immature neuronal tissue, either cultured fetal neurons or postnatal hippocampal slices, but was absent in adult brain. These observations indicate that Na+ channel internalization is triggered by Na+ influx into neurons and may be involved in the control of electrical activity during development.

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Aging Amphotericin B Animals Animals, Newborn Brain Cells, Cultured Down-Regulation Fetus Hippocampus Neurons Rats Saxitoxin Scorpion Venoms Sodium Channels Tetrodotoxin Journal Article

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B Dargent, C Paillart, E Carlier, G Alcaraz, M F Martin-Eauclaire, F Couraud. 1994. Sodium channel internalization in developing neurons.. https://doi.org/10.1016/0896-6273(94)90035-3

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