The mitochondrial KATP channel opener BMS-191095 induces neuronal preconditioning

Bela Kis, Krisztina Nagy, James A. Snipes, Nishadi C. Rajapakse, Takashi Horiguchi, Gary J. Grover, David W. Busija

Research output: Contribution to journalArticlepeer-review

63 Citations (Scopus)


BMS-191095, reportedly a selective mitoKATp channel opener which is free from the known side effects of the prototype mitoKATP channel opener diazoxide, induced acute and delayed preconditioning against glutamate excitotoxicity and delayed preconditioning against oxygen-glucose deprivation in primary cultures of rat cortical neurons. BMS-191095 dose dependency depolarized the mitochondria, increased the phosphorylation of PKC isoforms, but had no detectable effects on the activation of MAP kinases and did not influence the expressions of HSP70 and Mn-SOD. In BMS-191095- preconditioned neurons the glutamate-induced free-radical production was abolished. Our data give the first evidence that selective opening of mitoK ATP channels with BMS-191095 leads to remarkable neuroprotection via mechanisms that involve mitochondrial depolarization, PKC activation and attenuated free radical production during neuronal stress.

Original languageEnglish
Pages (from-to)345-349
Number of pages5
Issue number2
Publication statusPublished - 2004 Feb 9
Externally publishedYes


  • BMS-191095
  • Channel
  • Free radicals
  • Glutamate
  • MitoK
  • Oxygen-glucose deprivation
  • Preconditioning
  • Protein kinase C

ASJC Scopus subject areas

  • Neuroscience(all)


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