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Comparison of norepinephrine induced and benzodiazepine induced augmentation of purkinje cell responses to gamma amino butyric acid

, : Comparison of norepinephrine induced and benzodiazepine induced augmentation of purkinje cell responses to gamma amino butyric acid. Journal of Pharmacology & Experimental Therapeutics 228(2): 257-267

The hypothesis that the benzodiazepines (i.e, flurazepam) and norepinephrine (NE) share a common mechanism to facilitate cerebellar Purkinje neuron responsiveness to ionotophoretically applied GABA was tested. Extracellular activity was recorded from Purkinje neurons in halothane-anesthetized rats from each of the following groups: naive, acute or chronic flurazepam treated; chronic demethylimipramine treated; and injected with 6-hydroxydopamine. Single unit responses to pulsatile (10 s duration at 45-s intervals) iontophoretic administration of GABA were examined before, during and after NE or flurazepam microiontophoresis in all treatment groups. Drug response histograms were generated and used to quantitate NE and flurazepam effects on spontaneous activity and GABA-induced inhibitory responses. Doses of GABA sufficient to produce depression of Purkinje cell activity in naive rat (4-40 nA) suppressed firing rate in all Purkinje cells tested in drug-treated animals. In contrast to its consistent GABA facilitating action in naive controls, iontophoretically applied flurazepam was ineffective in augmenting GABA-induced suppression of Purkinje cell discharge in acute and chronic flurazepam-treated animals. Although GABA facilitation by NE was unaffected by acute systemic administration of a benzodiazepine, chronic treatment with flurazepam produced a subsensitivity to the noradrenergic GABA facilitating effects. Within 48 h of withdrawal from chronic benzodiazepine treatment, both NE and flurazepam again enhanced GABA-induced suppression of Purkinje cell discharge routinely. Chronic demethylimipramine treatment as well as iontophoresis of the blocking agents sotalol and fluphenazine which previously blocked or reduced NE-mediated enhancement of GABA actions, were ineffective in altering the facilitating effect of flurazepam on GABA. 6-Hydroxydopamine pretreatment had no effect on GABA augmentation by flurazepam. Although flurazepam apepars to act independently from the noradrenergic receptor system in augmenting GABA-induced depression of Purkinje cell discharge, a reversible subsensitivity to the GABA facilitating effects of both flurazepam and NE can be produced by chronic treatment with this benzodiazepine. On the basis of this cross-subsensitivity to NE and flurazepam actions, these 2 agents might enhance GABA inhibitory actions by a common biophysical mechanism subsequent to noradrenergic receptor activation.


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