SODIUM-CHANNEL INTERNALIZATION IN DEVELOPING NEURONS

被引：55

作者：

DARGENT, B ^{[1
]}

PAILLART, C ^{[1
]}

CARLIER, E ^{[1
]}

ALCARAZ, G ^{[1
]}

MARTINEAUCLAIRE, MF ^{[1
]}

COURAUD, F ^{[1
]}

机构：

[1] FAC MED SECTOR NORD, INST JEAN ROCHE, CNRS, URA 1455, F-13916 MARSEILLE 20, FRANCE

来源：

NEURON | 1994年 / 13卷 / 03期

关键词：

D O I：

10.1016/0896-6273(94)90035-3

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Neurotoxin-induced activation of voltage-dependent Na+ channels provoked rapid (t(1/2) = 15-20 min) channel down-regulation in cultured rat brain neurons, resulting in a 50%-70% decrease in [H-3]saxitoxin and I-125-alpha-scorpion toxin binding capacities as well as a decrease in Na+ peak current. Experiments using I-125-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.

引用

页码：683 / 690

页数：8

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