Voltage-dependent Na+/K+ ion channel blockade fails to ameliorate behavioral deficits after traumatic brain injury in the rat

X. Di, Bruce G Lyeth, R. J. Hamm, M. R. Bullock

Research output: Contribution to journalArticle

12 Scopus citations

Abstract

Traumatic brain injury (TBI) induces massive, transient ion flux, after impact. This may be via agonist gated channels, such as the muscarinic, cholinergic or NMDA receptor, or via voltage-dependent channels. Pharmacological blockade of the former, is neuroprotective in most TBI models, but the role of voltage-dependent Na+/K+ channels has not been tested. We have therefore tested the hypothesis that intraventricular tetrodotoxin (TTX) (20 μl, 5 mM) induced blockade of post-TBI ion flux will prevent cytotoxic cell swelling, Na+ and K+ flux, and behavioral deficit. Microdialysis demonstrated blockade of [K+]d flux in the TTX group compared to controls. Behavioral evaluation of motor (days 1-5) and memory function (days 11-15) after TBI revealed no beneficial effect in the TTX group compared to controls. Thus, although evidence of reduced ionic flux was demonstrated in the TTX group, memory and behavior were unaffected, suggesting that agonist-operated channel-mediated ion flux is more important after TBI.

Original languageEnglish (US)
Pages (from-to)497-504
Number of pages8
JournalJournal of Neurotrauma
Volume13
Issue number9
StatePublished - Sep 1996
Externally publishedYes

Keywords

  • behavioral performance
  • fluid percussion
  • microdialysis
  • neurotrauma
  • tetrodotoxin (TTX)
  • traumatic brain injury
  • voltage- gated channel

ASJC Scopus subject areas

  • Clinical Neurology
  • Neuroscience(all)

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