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Vigabatrin
Author(s) -
BenMenachem Elinor
Publication year - 1995
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1111/j.1528-1157.1995.tb06003.x
Subject(s) - vigabatrin , gaba transaminase , gabaa receptor , inhibitory postsynaptic potential , neurotransmitter , pharmacology , gaba receptor , gamma aminobutyric acid , neuroscience , gaba receptor antagonist , glutamate receptor , agonist , chemistry , mechanism of action , epilepsy , receptor , bicuculline , anticonvulsant , biology , central nervous system , glutamate decarboxylase , biochemistry , enzyme , in vitro
Summary: γ‐Aminobutyric acid (GABA) was first proposed as a putative inhibitory neurotransmitter by Elliot and van Gelder in 1958. Since then, numerous efforts have been made to find ways to increase GABA at its receptor sites, based on the findings that decreased GABA results in convulsions in animals and that agents enhancing GABA‐mediated functions can have antiepi‐leptic effects. However, the relationship between GABA levels and seizures is not simple. Seizures can occur even in the presence of elevated GABA levels. Indeed, it is possible that regional biochemical differences in the brain can be important. The antiepileptic effects of GABA depend on the mechanism whereby GABA‐mediated inhibition is enhanced. Since the 1970s, several compounds have been developed that are designed to act in some manner on the GABA system. These compounds affect GABA‐mediated inhibition at different levels and appear to have varied effects, depending on their mechanism of action. To date, specific antiepileptic drugs (AEDs) with potential GABA‐inhibitory effects have been designed either to have GABA agonist properties, to inhibit GABA catabolism, to inhibit GABA uptake, or to facilitate GABA release or facilitate GABA A receptor activity. Vigabatrin (VGB) was designed specifically to inhibit GABA transaminase and thereby increase the availability of GABA in the brain. Study data and clinical experience over the past 14 years have demonstrated VGB to be an effective AED.