Abstract
Double-labeling immunocytochemical techniques and confocal microscopy were used to quantify possible differences in the degree of colocalization of glutamate ionotropic receptor subunits between non-spiking and spiking neocortex removed from temporal lobe epileptic patients. Spiking neocortex was characterized by laminar-specific changes in the number of cells immunoreactive for NMDAR1, GluR2/3 and GluR5/6/7 subunits, as well as the percentage of cells which colocalized various combinations of these receptors. These changes may lead to profound modifications in the functioning of excitatory synaptic circuits in spiking cortex.
Published Version
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