2-Chloroadenosine attenuates NMDA, kainate, and quisqualate toxicity

Neurosci Lett. 1991 May 27;126(2):191-4. doi: 10.1016/0304-3940(91)90551-4.

Abstract

Excitatory amino acid (EAA)-induced cell death in the striatum is dependent upon intact glutamatergic afferents arising from the cerebral cortex. Through a mechanism possibly related to inhibition of glutamate release, adenosine receptor agonists attenuate EAA induced toxicity in the rat striatum. In the present study, we examined whether 2-chloroadenosine (2CLA), a stable adenosine analog, protects against toxicity induced by kainate (KA), quisqualate (QUIS), N-methyl-D-aspartate (NMDA), and ibotenate (IBO). In vivo intrastriatal injections of 2CLA (50 nmol) with each EAA tested provided a partial but significant protective effect versus injection of the EAA alone, as measured by striatal concentrations of gamma-aminobutyric acid (GABA) and substance P-like immunoreactivity (SP-LI). These results show that 2CLA attenuates both NMDA- and non-NMDA-mediated neuronal cell death.

Publication types

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

MeSH terms

  • 2-Chloroadenosine / pharmacology*
  • Animals
  • Corpus Striatum / drug effects*
  • Corpus Striatum / pathology
  • Injections
  • Kainic Acid / antagonists & inhibitors
  • Kainic Acid / toxicity*
  • Male
  • N-Methylaspartate / antagonists & inhibitors
  • N-Methylaspartate / toxicity*
  • Quisqualic Acid / antagonists & inhibitors
  • Quisqualic Acid / toxicity*
  • Rats
  • Rats, Inbred Strains

Substances

  • 2-Chloroadenosine
  • N-Methylaspartate
  • Quisqualic Acid
  • Kainic Acid