The administration of quinidine derivatives is utilized to monitor various skin and mucosal reactions. In certain cases, a papulopurpuric eruption can arise in patients (without thrombocytopenia) who are intermittently taking quinidine phenylethyl barbiturate and upon its reintroduction. Barbiturates exert their effects by binding to the GABAA receptor, targeting either the alpha or beta subunit. These binding sites are distinct from both GABA itself and the benzodiazepine binding site. Similar to benzodiazepines, barbiturates enhance the impact of GABA at this receptor. This interaction with the GABAA receptor results in decreased input resistance, suppression of burst and tonic firing, particularly in ventrobasal and intralaminar neurons. Concurrently, it increases burst duration and the average conductance at individual chloride channels. Consequently, this enhances the amplitude and duration of inhibitory postsynaptic currents. Beyond their GABAergic action, barbiturates also inhibit the AMPA receptor, a subtype of glutamate receptor. Notably, glutamate serves as the primary excitatory neurotransmitter in the mammalian central nervous system.

Quinidine barbiturate Pathway References