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Inhibitory interneurons in the brain provide the balance to excitatory signaling. On the basis of brain imaging and human genetics, a deficit in GABAergic inhibition (GABA, γ-aminobuiyric acid) has been identified as contributing to the pathophysiology of anxiety disorders, epilepsy, and schizophrenia. Therapeutically, GABAA receptors play a major role as targets for benzodiazepine drugs. The therapeutic relevance of the multitude of structurally diverse GABAA receptor subtypes has only recently been identified. α1-GABAA receptors were found to mediate sedation, anterograde amnesia, and part of the seizure protection of these drugs, whereas α2-GABAA receptors, but not α3-GABAA receptors, mediate anxiolysis. Rational drug targeting to specific receptor subtypes has now become possible. Only restricted neuronal networks will be modulated by the upcoming subtype-selective drugs. For instance, anxiolytics devoid of drowsiness and sedation promise more sophisticated interventions in anxiety disorders. A new pharmacology of the benzodiazepine site is on the horizon.

Pathophysiological aspects of diversity in neuronal inhibition: a new benzodiazepine pharmacology