GABAergic modulation of benzodiazepine binding site sensitivity.

摘要: ALTHOUGH neurophysiological, behavioural and biochemical evidence suggests that benzodiazepines (BZ) may affect several neuronal systems within the central nervous system (CNS), recent studies indicate some of these effects result from a specific interaction with GABAergic transmission1. The precise mechanism this remains in doubt, as facilitation transmission2, potentiation inhibition3,4, direct activation γ-aminobutyric acid (GABA) receptors5, antagonism GABA-mediated inhibition have all been attributed to benzodiazepines6,7. In laboratory8, both systemic iontophoretic administration BZs potentiated an inhibitory response produced by GABA dorsal raphe nucleus—suggesting was mediated through change post-synaptic receptor. addition, binding using 3H-diazepam indicated high affinity site which be relevant pharmacological actions BZ brain9. study, we show can modulate responsiveness since addition cortical membranes vitro results increased for its ligand. This effect is mimicked analogue, muscimol10, antagonised antagonist, (+)bicuculline.