The sedative effects of benzodiazepine receptors are due to activation of α-1 subunits of GABA receptors.
The anxiolytic activity associated with the benzodiazepine is due to α-2 subunit activity.
The GABAA receptor is large, providing attachment sites for GABA, benzodiazepines, barbiturates, etomidate, propofol, and alcohol.
This property explains the pharmacologic synergy of these substances and the risks of combined overdose and cross-tolerance.
Benzodiazepines have a ceiling effect in production of GABAergic neurotransmission.
It is for this reason we see that the benzodiazepines, barbiturates, and alchohol can produce synergistic effects to increase GABAA benzodiazepine receptors mediated inhibition in the CNS.
On the other hand, the gamma-aminobutyric acid (GABA) receptor channel allows chloride ions to permeate into the cell, and hypcrpolarizes the cell membrane. Many drugs (phenytoin and benzodiazepines) act by modifying the function of receptor channels.
Opening of the potassium channels allows potassium ions to leak out of the cell and thus hyperpolarizes the cell membrane e.g. sulfonylurea receptor.
The exact mechanism of antianxiety action is not known though they act at many levels of the neural axis. Experimentally, they have been shown to act on the limbic system, the hypothalamus and the brain stem reticular system.
They bind to BDZ benzodiazepine receptors and facilitate the action of GABA. Benzodiazepines also reduce the turnover of brain 5-HT and noradrenaline.