Chloride flow and fast inhibition at the GABA-A receptor
The GABA-A receptor is a ligand-gated ion channel assembled from five subunits, most commonly two alpha, two beta, and one gamma. When GABA binds at the interface between alpha and beta subunits, the central pore opens and chloride ions flow according to their electrochemical gradient. In mature neurons this usually drives the membrane potential more negative, making the cell less likely to fire. This is the brain's main mechanism for fast synaptic inhibition.
Because the response depends on a channel opening directly, GABA-A inhibition is rapid, on the order of milliseconds, which distinguishes it from the slower, G-protein-coupled GABA-B receptor.
Where benzodiazepines, alcohol, and sleep compounds bind
Many sedating substances do not activate the receptor themselves; they bind at separate allosteric sites and increase the channel's response to the brain's own GABA. Benzodiazepines act at the alpha-gamma interface and raise the frequency of channel opening, while barbiturates prolong opening. Alcohol, neurosteroids, and some plant compounds also modulate the receptor at distinct sites.
This is educational background on receptor pharmacology, not medical or dosing advice. Drugs acting on GABA-A receptors can interact dangerously and should only be used under professional supervision.