Current theories about the mechanisms of benzodiazepines and neuroleptic drugs.
The data reviewed above are the basis for the models of drug action proposed by neuropharmacologists. Mechanisms of benzodiazepine action are currently attributed to increased inhibitory neurotransmission. Costa and Guidotti26 proposed that anticonvulsant and sedative properties are a consequence of enhanced inhibitory neurotransmission mediated by GABA. Muscle relaxation may result from glycinemimetic actions of benzodiazepines in the spinal cord. Antianxiety mechanisms may be effects of both glycine- and GABA-mediated inhibition of specific neuronal pathways in the brainstem and brain (see fig. 2). Antipsychotic and extrapyramidal effects of neuroleptic drugs may be a consequence of their action at dopaminergic receptors.
D014150:Antipsychotic Agents / Q000494:pharmacology*; D001569:Benzodiazepines / Q000494:pharmacology*; D001665:Binding Sites; D001921:Brain / Q000378:metabolism; D004298:Dopamine / Q000502:physiology; D005968:Glutamate Decarboxylase / Q000378:metabolism; D005998:Glycine / Q000502:physiology; D006801:Humans; D018377:Neurotransmitter Agents / Q000494:pharmacology; D011954:Receptors, Dopamine / Q000187:drug effects; D011955:Receptors, Drug / Q000378:metabolism; D013570:Synaptic Membranes / Q000378:metabolism; D009435:Synaptic Transmission / Q000187:drug effects*; D005680:gamma-Aminobutyric Acid / Q000502:physiology
D014150:Antipsychotic Agents; D018377:Neurotransmitter Agents; D011954:Receptors, Dopamine; D011955:Receptors, Drug; D001569:Benzodiazepines; D005680:gamma-Aminobutyric Acid; D005968:Glutamate Decarboxylase; D005998:Glycine; D004298:Dopamine