ABSTRACT
This chapter focuses on the antiepileptic activity of barbiturates and potential mechanism by which barbiturates like phenobarbital may produce their anticonvulsant effect. It also focuses on the interaction of barbiturates with Gamma Aminobutyric Acid (GABA)A ergic transmission in the mammalian central nervous system. Antiepileptic drugs are routinely used to control different forms of seizure disorders. Epilepsy is a nonhomogenous group of disorders, including primary generalized epilepsy and myoclonic seizure disorders. Barbiturates have varying effects on benzodiazepine binding. Most of the depressant barbiturates enhance [3H] benzodiazepine agonist binding in brain membranes. Barbiturates apparently act allosterically, increasing the affinity of benzodiazepine agonists for their binding sites, presumably, by decreasing the rate of the dissociation. The structural differences between barbiturates and picrotoxin-like cage convulsants further supports the differences in binding characteristics between picrotoxin-like cage convulsants and barbiturates. The enhancement of GABAergic transmission by barbiturates has been well documented using both biochemical and electrophysiological approaches.
