Toxicology
At low doses, barbiturates bind to GABA-sensitive ion channels in CNS, leading increased influx of chloride ions into cell membranes where they produce hyperpolarization of post synaptic neurone (Lafferty KA, 2014
Barbs prolong the opening of the chloride ion channels, which in turn increases the efficacy of GABA activity.
The barbiturates bind to Beta subunit of GABA-A receptor ionophore complex thus potentiating and promoting inhibitor effects of GABA. However, at sufficiently high doses, barbiturates independently stimulates GABA-A (a theoretical benefit in treating of seizures induced by toxins that deplete GABA) in addition to binding to other . . .
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