2-Chloroadenosine attenuates NMDA, kainate, and quisqualate toxicity

doi:10.1016/0304-3940(91)90551-4

Neuroscience Letters

Volume 126, Issue 2, 27 May 1991, Pages 191-194

https://doi.org/10.1016/0304-3940(91)90551-4 Get rights and content

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 γ-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.

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2-Chloroadenosine attenuates NMDA, kainate, and quisqualate toxicity

Abstract

Neurosci. Lett.

Arch. Biochem. Biophys.

Biochem. Pharmacol.

Neurosci. Lett.

Eur. J. Pharmacol.

Neurosci. Lett.

Int. Rev. Neurobiol.

J. Neurosci. Methods

Biochem. Pharmacol.

Neurosci. Lett.

Eur. J. Pharmacol.

Neuropharmacology

Neurosci. Lett.

Brain Res.

Brain Res.

Neurosci. Lett.

Neurosci. Lett.

Eur. J. Pharmacol.