Abstract
Acute cocaine injection to rats is known to induce the expression of immediate early genes in the forebrain, the effect being primarily mediated by the dopaminergic system. We examined the effect of the anesthetics ketamine and propofol on cocaine-induced egr-1 mRNA expression. Using in situ hybridization, we show that both compounds did not induce egr-1 gene by themselves, but were able to dose-dependently reduce cocaine-induced egr-1 mRNA synthesis in the nucleus accumbens, caudate-putamen and cingulate cortex. Our data suggest that in addition to glutamate NMDA receptors, propofol may act via GABA A receptors or ion channels.
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