Voltage-sensitive calcium channels mediate calcium entry into cultured mammalian sympathetic neurons following neurite transection

Document Type

Article

Abstract

Calcium ion entry following mechanical neurite transection was examined in cultured sympathetic neurons loaded with the Ca2+ indicator fluo-3. Neurite transection produced a rapid [Ca2+](i) rise in the cell soma which preceded any [Ca2+](i) rise in the neurite (n = 30). Blacking sodium channels with tetrodotoxin had no effect on the Ca2+ rise, but inactivating voltage-sensitive Ca2+ channels by bath-applying 140 mM potassium prior to the transection, and the simultaneous application of nimodipine and ω-conotoxin GVIA, channels, respectively, considerably attenuated the Ca2+ rise in the soma and neurites. These data entry following mechanical neurite transection occurs via non-specific influx pathways produced by cell-membrane disruption and provide direct evidence in mammalian neurons that immediate, traumatically-induced, increases in neuronal [Ca2+](i) are amenable to pharmacological manipulation.

Keywords

Axotomy, Calcium, Calcium channel, Confocal microscopy, Neurotoxicity, Sympathetic neuron, Trauma

Publication Date

5-6-1996

Publication Title

Brain Research

ISSN

00068993

Volume

719

Issue

1-2

First Page

239

Last Page

246

PubMed ID

8782889

Digital Object Identifier (DOI)

10.1016/0006-8993(96)00125-4

Link to Full Text

Share

COinS