Amobarbital, a derivative of barbiturate, finds application in inducing sedation during medical procedures, short-term management of insomnia, and acute control of refractory tonic-clonic seizures. As a barbiturate possessing hypnotic and sedative attributes (though not antianxiety effects), its adverse reactions primarily stem from dose-related central nervous system depression, and there exists a substantial risk of dependence with prolonged use. Amobarbital, similar to all barbiturates, functions through binding to the GABAA receptor at either the alpha or beta subunit. These binding sites are distinct from GABA itself and also separate from the benzodiazepine binding site. Comparable to benzodiazepines, barbiturates enhance GABA's impact at this receptor. This interaction with the GABAA receptor reduces input resistance, suppresses burst and tonic firing, particularly in ventrobasal and intralaminar neurons. Concurrently, it extends burst duration and the average conductance at individual chloride channels, ultimately raising both the amplitude and decay time of inhibitory postsynaptic currents. Beyond their GABAergic effect, barbiturates also hinder the AMPA receptor, a subtype of the glutamate receptor. Notably, glutamate serves as the principal excitatory neurotransmitter in the mammalian central nervous system. Additionally, Amobarbital seems to bind to neuronal nicotinic acetylcholine receptors.

Amobarbital Pathway References