Cocaine depresses GABA(A) current of hippocampal neurons

Jiang Hong Ye, Philip L. Liu, Wen Hsien Wu, Joseph J. McArdle

Research output: Contribution to journalArticlepeer-review

41 Scopus citations

Abstract

Although blockade of dopamine re-uptake and the resulting elevation of excitatory agonists is commonly thought the primary mechanism of cocaine- induced seizures, it is possible that other neurotransmitters such as γ- aminobutyric acid (GABA) are involved. To examine this possibility, the effects of cocaine on the whole cell GABA current (1(GABA)) of freshly isolated rat hippocampal neurons were investigated with the patch-clamp technique. Preincubation or acute application of cocaine reversibly suppressed I(GABA). The IC50 was 127 μM when cocaine was applied before the application of GABA. The concentration-response relations of cocaine in various GABA concentrations revealed that cocaine inhibited I(GABA) non- competitively. This effect of cocaine appeared to be independent of voltage. The present study suggests that the GABA receptor/channel complex is also a target for cocaine's action. The suppression of I(GABA) may contribute to cocaine-induced seizures.

Original languageEnglish (US)
Pages (from-to)169-175
Number of pages7
JournalBrain research
Volume770
Issue number1-2
DOIs
StatePublished - Oct 3 1997
Externally publishedYes

All Science Journal Classification (ASJC) codes

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

Keywords

  • Cocaine
  • Hippocampal neuron
  • Local anesthetic toxicity
  • Patch clamp
  • Seizure
  • Whole cell GABA(A) current
  • γ-Aminobutyric acid receptor/channel

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