Neurotransmission in epilepsy.
Some evidence indicates that in some types of focal epilepsy the enhanced excitability is due in part to impaired gamma-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 GABA/benzodiazepine (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.
Institute of Epileptology, Department of Neurology, Institute of Psychiatry, London, UK.
B S
BS
Meldrum
D000818:Animals; D004827:Epilepsy / Q000473:pathology* / Q000503:physiopathology; D059330:GABAergic Neurons / Q000502:physiology; D018698:Glutamic Acid / Q000378:metabolism; D006801:Humans; D009433:Neural Inhibition / Q000502:physiology; D009435:Synaptic Transmission / Q000502:physiology*
D018698:Glutamic Acid