Feb 1, 1984

Comparison of norepinephrine- and benzodiazepine-induced augmentation of Purkinje cell responses to gamma-aminobutyric acid (GABA)

The Journal of Pharmacology and Experimental Therapeutics
B D WaterhouseD J Woodward


The hypothesis tested in the present study was that the benzodiazepines (i.e., flurazepam) and norepinephrine (NE) share a common mechanism to facilitate cerebellar Purkinje neuron responsiveness to iontophoretically applied gamma-aminobutyric acid (GABA). Extracellular activity was recorded from Purkinje neurons in halothane-anesthetized rats from each of the following groups: 1) naive, 2) acute or chronic flurazepam treated, 3) chronic desmethylimipramine treated and 4) injected with 6-hydroxydopamine. Single unit responses to pulsatile (10 sec duration at 45-sec 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 rats (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...Continue Reading

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Mentioned in this Paper

Drug Response
Depression, Chemical
August Rats
Purkinje Cells
Synaptic Transmission

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