The GABA-A receptor complex is a post-synaptic ligand-gated chloride ion channel. In the absence of GABA in the synapse, the chloride ion channel is closed. However, with the binding of GABA, the channel opens, allowing chloride ions to flow into the cell with the concentration gradient. However as this is also against the electrochemical gradient, the result is a further drop in the transmembrane potential away from the threshold for the propagation of an action potential.
In the presence of many CNS active agents such as benzodiazepines, barbiturates, and alcohol, the binding of GABA is enhanced. The influx of chloride ions is greater and a further reduction of the transmembrane potential occurs.
medium; background-color: #e4eaff;">Lastly some drugs act at specific subunit subtypes of the complex. Benzodiazepines are thought to work at the α2 or α3 subunit, whereas zolpidem, a drug used for sedation is thought to be specific for the α1 subunit.
The GABA-A chloride ion channel is composed of five subunits that have different configurations throughout the brain.
Extra info: These different configurations may explain the variety of actions and susceptibility of benzodiazepines in the brain.
Benzodiazepines, barbiturates and alcohol share the same binding site on the GABA-A chloride ion channel.
Extra info: Although they all effect the GABA-A receptor, they do so in different locations on the channel.
The pharmacological effects of benzodiazepines and alcohol can be additive.
Extra info: Because benzodiazepines and alcohol have different binding sites and their effect on the ion channel different, their actions on the membrane potential can be additive.