Anxiety as a state of diminished gabaergic neurotransmission resulting from too frequent recruitment of gabaergic neurons: A neurophysiological model

Abstract

• 1.

  1. All of the most commonly used antianxiety drugs (benzodiazepines, barbiturates, ethanol) selectively enhance GABA-mediated neurotransmission.

• 2.

  2. The degree of GABA-potentiation produced by benzodiazepines correlates well with their relative affinities for the benzodiazepine receptor.

• 3.

  3. Repetitive stimulation of the recurrent inhibitory GABAergic pathway in rat hippocampus leads to a remarkable reduction of the effectiveness of GABA; this “disinhibition” is counteracted by antianxiety drugs.

• 4.

  4. A neurophysiological model is proposed, conceptualizing anxiety as the by-product of hypervigilance occurring in frequencies higher than those that the GABAergic system can accommodate, before “fading” or “desensitization” occurs.