Bunazosin hydrochloride reduces glutamate-induced neurotoxicity in rat primary retinal cultures

Brain Res. 2004 Apr 2;1003(1-2):130-7. doi: 10.1016/j.brainres.2003.12.030.

Abstract

To study neuroprotective effects of bunazosin hydrochloride which is an alpha(1)-adrenoceptor antagonist used as an ocular hypotensive drug compared to other alpha(1)-adrenoceptor antagonists, and its mechanism of action. We evaluated the neuroprotective effects of bunazosin hydrochloride or seven other alpha(1)-adrenoceptor antagonists against glutamate-induced cell death in rat primary retinal cultures. We also evaluated the binding inhibition of bunazosin hydrochloride for 24 different receptors/channels and its effects on the Na(+) influx into cells induced by veratridine or glutamate. Bunazosin hydrochloride significantly inhibited glutamate-induced cell death at concentrations of 1 and 10 microM. Cells were also protected when treated with some alpha(1)-adrenoceptor antagonists, but not by the others. Bunazosin hydrochloride showed a high inhibition for Na(+) channels and inhibited the Na(+) influx induced by veratridine or glutamate. These findings indicate that in retinal cultures bunazosin hydrochloride has a neuroprotective effect against glutamate-induced cell death and that the inhibition of Na(+) channels by bunazosin hydrochloride may be partly responsible for this effect.

Publication types

  • Comparative Study

MeSH terms

  • Animals
  • Brain / drug effects
  • Brain / metabolism
  • Cell Death / drug effects
  • Cell Death / physiology
  • Cells, Cultured
  • Dose-Response Relationship, Drug
  • Female
  • Glutamic Acid / toxicity*
  • Pregnancy
  • Protein Binding / drug effects
  • Protein Binding / physiology
  • Quinazolines / pharmacology*
  • Rats
  • Rats, Wistar
  • Retina / drug effects*
  • Retina / metabolism

Substances

  • Quinazolines
  • Glutamic Acid
  • bunazosin