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Updated: May 17, 2026

Electroconvulsive Seizures in Rats and Fractionation of Their Hippocampi to Examine Seizure-induced Changes in Postsynaptic Density Proteins
Published on: August 15, 2017
Neurotransmission in epilepsy
1Institute of Epileptology, Department of Neurology, Institute of Psychiatry, London, UK.
Abstract:
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.
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