Neural mechanisms of benzodiazepine actions.
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.
D000613:Aminobutyrates / Q000378:metabolism*; D014151:Anti-Anxiety Agents / Q000494:pharmacology*; D001569:Benzodiazepines; D002395:Catecholamines / Q000378:metabolism; D002531:Cerebellum / Q000187:drug effects; D006801:Humans; D008032:Limbic System / Q000187:drug effects; D009433:Neural Inhibition / Q000187:drug effects*; D009474:Neurons / Q000187:drug effects / Q000502:physiology; D011955:Receptors, Drug / Q000187:drug effects; D013116:Spinal Cord / Q000187:drug effects; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
D000613:Aminobutyrates; D014151:Anti-Anxiety Agents; D002395:Catecholamines; D011955:Receptors, Drug; D001569:Benzodiazepines; D005680:gamma-Aminobutyric Acid