PMID: 9551769Apr 29, 1998Paper

Methamphetamine modulates GABA-induced electrophysiological depression by alternating noradrenergic actions in cerebellar Purkinje neurons

Psychopharmacology
C H Jeng, Y Wang

Abstract

Previous studies have indicated that gamma-aminobutyric acid (GABA)-induced electrophysiological responses can be enhanced by noradrenaline (NE) acting via beta-adrenergic receptors. Methamphetamine (MA) has been reported to be a noradrenergic releasing agent. In the present study, we examined the interaction of MA and GABA in cerebellar Purkinje neurons of urethane-anesthetized rats. We found that local application of MA did not potentiate GABA-induced electrophysiological depressions in Purkinje neurons. Since MA may act indirectly or directly on alpha or beta noradrenergic receptors, we further examined the interactions of MA with selective noradrenergic antagonists. We found that after blocking alpha-adrenergic receptors with prazocin, MA significantly facilitated GABA responses. On the other hand, co-administration of timolol with MA did not attenuate GABA-induced neuronal depressions. To examine further the interactions between alpha and beta receptors in modulating GABA response, we found that stimulation of alpha-adrenergic receptors in the absence of beta receptor activation, such as by application of the alpha-agonist phenylephrine alone, did not decrease GABA-induced inhibition. However, stimulation of alpha-adrenerg...Continue Reading

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