The binding sites for GABA are located between adjacent
subunits,and the binding pocket for benzodiazepines (the
of the GABA
receptor) is between an
Benzodiazepines and other sedative-hypnotics have a low affinity for GABA
GABA (gamma-aminobutyric acid) is the major inhibitory neurotransmitter in thecentral nervous system.
Benzodiazepines appear to increase the efficiency of GABAergic synapticinhibition.
The benzodiazepines do not substitute for GABA but appear to enhance GABA'seffects allosterically (by conformational change) without directly activating GABA
receptors or opening the associated chloride channels. The enhancement in chlorideion conductance induced by the interaction of benzodiazepines with GABA takes theform of an increase in the
of channel-opening events .
Barbiturates also facilitate the actions of GABA but
in contrast to benzodiazepines
they appear to increase the
of the GABA-gated chloridechannel openings. At high concentrations, the barbiturates may also be GABA-mimetic, directly activating chloride channels. Barbiturates are less selective in their