GABA
GABA, short for gamma-aminobutyric acid, is the brain's main 'stop' signal. If excitatory messengers tell neurons to fire, GABA tells them to hold back. Roughly speaking it is the brake pedal of the central nervous system, keeping electrical activity from running away into overexcitement or seizures.
GABA is the chief inhibitory neurotransmitter in the brain. It acts mainly on two receptor types: GABA-A, a fast ligand-gated chloride channel whose opening hyperpolarizes the neuron and makes it less likely to fire, and GABA-B, a slower G-protein-coupled receptor. The GABA-A receptor is the target that explains a huge swath of CNS pharmacology.
Many sedating drugs work by amplifying GABA's effect at GABA-A: benzodiazepines increase how often its channel opens, barbiturates prolong how long it stays open, and general anaesthetics, alcohol, and certain antiepileptics also act here. This shared target is why these drugs add together dangerously.
Because GABA inhibition is so central, both too little and too much cause trouble. Too little inhibition tips toward anxiety and seizures; too much, from drug overdose, sinks the brain into coma and stops breathing.
When a patient takes a benzodiazepine and drinks alcohol, both enhance GABA-A inhibition on top of each other, which can deepen sedation to the point of stopping breathing.
Shared action at GABA-A underlies dangerous depressant interactions.
The GABA-A receptor is a beautiful example of one drug target shared by many drug classes — knowing it explains benzodiazepines, barbiturates, Z-drugs, alcohol, and several anaesthetics all at once.