barbiturate
A barbiturate is an older, powerful sedative that presses the brain's inhibitory brake so hard it can hold it down on its own. Where a benzodiazepine merely amplifies the body's natural signal, a barbiturate can keep working even when that signal is weak — which makes it stronger, but also more dangerous.
Barbiturates act at the GABA-A receptor, but instead of increasing how often the chloride channel opens, they prolong how long it stays open once opened. At higher concentrations they can open the channel directly without GABA at all. This GABA-independent action is why their dose-response curve has no real ceiling: pushing the dose keeps deepening CNS depression toward coma and fatal respiratory arrest.
Once central to anaesthesia, sleep, and seizure care, barbiturates have largely been replaced by safer benzodiazepines. They survive in a few niches: phenobarbital for some seizures, thiopental for rapid anaesthesia induction, and use in lethal contexts. They are also strong inducers of liver cytochrome P450 enzymes, speeding the metabolism of many co-administered drugs.
The narrow gap between an effective dose and a lethal one — a low therapeutic index — combined with high dependence potential is why these drugs are now used so sparingly and with great caution.
Phenobarbital, a long-acting barbiturate, is still used as an inexpensive antiepileptic in some settings, though it must be dosed carefully because of its narrow therapeutic index.
Barbiturates persist mainly where cost or specific properties outweigh their risks.
The key contrast: benzodiazepines increase the frequency of GABA-A channel opening, while barbiturates prolong its duration and can open it without GABA — the reason barbiturates are far deadlier in overdose.