Inhibitory, GABAergic nerve terminals decrease at sites of focal epilepsy.
Using an immunocytochemical method for the localization of the gamma-aminobutyric acid (GABA) synthesizing enzyme, glutamic acid decarboxylase (GAD), we have observed GABAergic nerve terminals distributed throughout all layers of normal monkey sensorimotor cortex. These terminals displayed ultrastructural characteristics that suggested that they arose from aspinous and sparsely spinous stellate neurons. In monkeys (Macaca mulatta and M. fascicularis) made epileptic by cortical application of alumina gel, a highly significant numerical decrease of GAD-positive nerve terminals occurred at sites of seizure foci indicating a functional loss of GABAergic inhibitory synapses. A loss of such inhibition at seizure foci could lead to epileptic activity of cortical pyramidal neurons.
D000818:Animals; D002262:Carboxy-Lyases / Q000378:metabolism*; D002540:Cerebral Cortex / Q000378:metabolism*; D004828:Epilepsies, Partial / Q000503:physiopathology*; D005968:Glutamate Decarboxylase / Q000378:metabolism*; D005971:Glutamates / Q000378:metabolism; D000882:Haplorhini; D008252:Macaca fascicularis; D008253:Macaca mulatta; D009044:Motor Cortex / Q000378:metabolism; D009411:Nerve Endings / Q000201:enzymology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D005971:Glutamates; D005680:gamma-Aminobutyric Acid; D002262:Carboxy-Lyases; D005968:Glutamate Decarboxylase