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

Rita Sattler, Michael Tymianski, Imran Feyaz, Mathias Hafner, Charles H. Tator

Research output: Contribution to journalArticlepeer-review

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.

Original languageEnglish (US)
Pages (from-to)239-246
Number of pages8
JournalBrain research
Volume719
Issue number1-2
DOIs
StatePublished - May 6 1996

Keywords

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

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology

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