Brain Disability As the Primary Clinical Effect

Neurophysiological studies show that the BZs potentiate the neuronal inhibition that is mediated by GABA. In doses used clinically, this results in a generalized suppression of both spontaneous and evoked electrical activity of the large neurons throughout all regions of the brain and spinal cord (Ballenger, 1995). 

The binding of BZs to the GABA receptors is most intense in the cerebral cortex. Some BZs, such as Xanax and Halcion, bind especially tightly, increasing their tendency to produce more intense sedation and hypnosis, and also more severe cognitive deficits, behavioral abnormalities, rebound, and withdrawal. 

People who use BZs to calm their anxiety will frequently use alcohol and other sedatives interchangeably for the same purpose, either in combination or at different times. As they switch from drug to drug, they tend to find little or no difference in the antianxiety effect. This confirms that BZs have no specificity for anxiety in comparison to other sedative/ hypnotic agents. 

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