Neural mechanisms of benzodiazepine actions
Abstract
Current experimental paradigms emphasize neurotransmitter-specific interactions to explain the behavioral effects of benzodiazepines. According to this approach the broad range of effects observed suggests the involvement of several transmitter systems without rigorously establishing that any single transmitter system or physiological synaptic function is either necessary or sufficient to express all benzodiazepine actions. Among the effects that occur, potentiation of amino acid-mediated presynaptic inhibition in the spinal cord and postsynaptic inhibitions elsewhere in the brain are attractive testable hypotheses. However, direct physiological evidence that benzodiazepines stimulate gamma-aminobutyric acid (GABA) or other amino acids specifically and exclusively is needed to corroborate this view.
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