Benzodiazepines (BDZs) bind to the gamma sub-unit of the GABA-A receptor. Their binding causes an allosteric (structural) modification of the receptor that results in an increase in GABA A receptor activity. BDZs do not substitute for GABA, which bind at the alpha sub-unit, but increase the frequency of channel opening events which leads to an increase in chloride ion conductance and inhibition of the action potential.1
Related content
Current evidence on the neurobiology of addictive behaviour highlights the transition from reward-driven to habitual drug use through alterations in mesolimbic dopamine, glutamatergic signalling, frontostriatal circuitry, and stress-related systems.
Functional neuroimaging studies commonly compare brain responses to substance-related cues versus neutral cues during fMRI or PET scanning and measure differential brain activation.
Recognition of addiction as a disorder of distributed brain circuits provides a framework for personalized assessment and treatment of addiction.