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Neurotransmission in Epilepsy
Author(s) -
Meldrum Brian S.
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.tb01649.x
Subject(s) - tiagabine , vigabatrin , epilepsy , glutamate receptor , gabaergic , inhibitory postsynaptic potential , neuroscience , anticonvulsant , pharmacology , nmda receptor , gabaa receptor , neurotransmission , excitatory postsynaptic potential , gaba transaminase , gaba receptor antagonist , chemistry , receptor , medicine , biology , bicuculline , glutamate decarboxylase , biochemistry , enzyme
Summary: Some evidence indicates that in some types of focal epilepsy the enhanced excitability is due in part to impaired γ‐aminobutyric acid (GABA)ergic inhibitory feedback. One form that this can take is impaired excitatory input to GABAergic interneurons. Enhanced excitatory receptor sensitivity, most characteristically involving N‐methyl‐D‐aspartate (NMDA) receptors, has been identified in kindled rodents and in focal epilepsy in humans. Drugs that enhance GABA‐mediated inhibition are anticonvulsant in many syndromes of generalized and focal epilepsy. Mechanisms through which this occurs include direct interaction with the GABAhenzodiazepine (BZD) receptor (BZDs, barbiturates, chlormethiazole), inhibition of GABA‐transaminase (vigabatrin, VGB) and blocking GABA uptake (tiagabine, TGB). Glutamate receptor antagonists (both NMDA and non‐NMDA antagonists) are potent anticonvulsants in many animal models of epilepsy. Whether pure glutamate receptor antagonists will have a clinical role as antiepileptic drugs (AEDs) remains to be established.