Long-term alterations in amino acid-induced ionic conductances in chronic epilepsy.

Extracellular free sodium (Na+)o and calcium (Ca2+)o concentration changes were measured in the rat motor cortex, using ion-selective microelectrodes. During ionophoretic applications of excitatory amino acids, decreases in (Na2+)o and in (Ca2+)o were observed. Ca2+ signals were not or very little modified by applications of tetrodotoxin while Na+ signals were slightly depressed, up to 20%. Laminar profile analysis revealed that, while the magnitude of Na+ signals was rather constant throughout the cortex, Ca2+ signals were largest in upper cortical layers. Lesioning and pharmacological experiments indicated that the corresponding permeabilities were most probably located on apical dendrites of pyramidal tract neurons. The relative amplitude of Na+ and Ca2+ signals induced by the release of the glutamate agonists N-methyl-D-aspartate, quisqualate and kainate and the shape of the laminar profile of such responses indicated that different ionic permeabilities located on different neurons underlie such responses. Similar experiments performed on chronic epileptogenic motor foci in rats indicated that the amino acid-induced ionic responses were altered. The significance of such alterations for epileptogenesis is discussed.