Abstract
ALTHOUGH benzodiazepines are widely used in routine medical practice their mechanism of action remains controversial1,2. Several authors have suggested that the action of benzodiazepines is to potentiate GABA-ergic processes in the central nervous system3–5. In addition, a number of studies have shown the effect of benzodiazepines to be antagonised by γ-amino-butyric acid (GABA) antagonists6,7. But, Steiner and Felix8 and Gähwiler9 have adopted the opposite view and reported that in the cerebellum and Deiters nucleus benzodiazepines antagonise the inhibitory action of GABA. On the other hand, Dray and Straughan6 have shown microiontophoretic applications of benzodiazepines to be inhibitory on the spontaneous and glutamate activity of neurones of the brain stem and were unable to confirm that benzodiazepines antagonise the action of GABA. Curtis et al.10 were also unable to confirm the results of Steiner and Felix8 on the neurones of the cerebellum and spinal cord. In the recent paper by Squires and Braestrup11 a direct interaction of benzodiazepines with GABA-receptors has been discarded. We have investigated the interaction between chlordiazepoxide (Librium) and GABA by observing the effects of simultaneous microiontophoretic application of both agents on the spontaneous and glutamate-evoked firing of single neurones of sensorimotor cortex of the rabbit and here we report that the actions of the two are synergistic.
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References
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KOZHECHKIN, S., OSTROVSKAYA, R. Are benzodiazepines GABA antagonists?. Nature 269, 72–73 (1977). https://doi.org/10.1038/269072a0
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DOI: https://doi.org/10.1038/269072a0
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