Clinical data have shown that various neurobiologic irregularities (eg, in the g-aminobutyric acid [GABA] and serotonin
systems) are associated with the development of anxiety.
Benzodiazepine receptors are attached to the GABAAreceptor. When benzodiazepine binds to its receptor, it increases
the effectiveness and prolongs the effect of GABA by increasing the amount of time the chloride channel is open.
This suppresses neuronal activity and regulates the release
of other neurotransmitters in GABA-rich areas of the brain,
especially in the hippocampus, substantia nigra, cerebellum,
and striatum. Altered sensitivity of central benzodiazepine
receptors have been suggested. Changes in the peripheral
benzodiazepine receptor binding have also been observed.
Long-term treatment with benzodiazepines has been shown
to increase the benzodiazepine peripheral binding sites
to normal levels, which suggests that dysregulation of peripheral benzodiazepine receptors may be involved in the
mechanism of GAD [21