Alpha7 nicotinic receptor mediated protection against ethanol-induced cytotoxicity in PC12 cells

Brain Res. 1999 Jan 16;816(1):225-8. doi: 10.1016/s0006-8993(98)01153-6.

Abstract

Ethanol caused a concentration-dependent loss of PC12 cells over a 24 h interval, accompanied by an increase in intracellular calcium. The specific alpha7 nicotinic receptor partial agonist DMXB attenuated both of these ethanol-induced actions at a concentration (3 microM) found previously to protect against apoptotic and necrotic cell loss. The alpha7 nicotinic receptor antagonist methylylaconitine blocked the neuroprotective action of DMXB when applied with but not 30 min after the agonist. These results indicate that activation of alpha7 nicotinic receptors may be therapeutically useful in preventing ethanol-neurotoxicity.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Aniline Compounds / metabolism
  • Animals
  • Benzylidene Compounds / pharmacology
  • Calcium / metabolism
  • Dose-Response Relationship, Drug
  • Ethanol / toxicity*
  • Flow Cytometry
  • Fluorescent Dyes / metabolism
  • Intracellular Fluid / metabolism
  • Nicotinic Agonists / pharmacology
  • Nicotinic Antagonists / pharmacology
  • PC12 Cells / drug effects
  • Pyridines / pharmacology
  • Rats
  • Receptors, Nicotinic / physiology*
  • Xanthenes / metabolism
  • alpha7 Nicotinic Acetylcholine Receptor

Substances

  • Aniline Compounds
  • Benzylidene Compounds
  • Chrna7 protein, rat
  • Fluorescent Dyes
  • Nicotinic Agonists
  • Nicotinic Antagonists
  • Pyridines
  • Receptors, Nicotinic
  • Xanthenes
  • alpha7 Nicotinic Acetylcholine Receptor
  • Fluo-3
  • Ethanol
  • 3-(2,4-dimethoxybenzylidene)anabaseine
  • Calcium