Changes in the colocalization of glutamate ionotropic receptor subunits in the human epileptic temporal lobe cortex

Exp Brain Res. 2001 Jun;138(3):398-402. doi: 10.1007/s002210100720.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Down-Regulation / physiology
  • Epilepsy / metabolism*
  • Epilepsy / pathology
  • Epilepsy / physiopathology
  • Glutamic Acid / metabolism
  • Humans
  • Immunohistochemistry
  • Male
  • Pyramidal Cells / metabolism*
  • Pyramidal Cells / pathology
  • Receptor, Metabotropic Glutamate 5
  • Receptors, AMPA / metabolism*
  • Receptors, Kainic Acid / metabolism*
  • Receptors, Metabotropic Glutamate / metabolism
  • Receptors, N-Methyl-D-Aspartate / metabolism*
  • Synaptic Transmission / physiology
  • Temporal Lobe / metabolism*
  • Temporal Lobe / pathology
  • Temporal Lobe / physiopathology
  • Up-Regulation / physiology

Substances

  • NMDA receptor A1
  • Receptor, Metabotropic Glutamate 5
  • Receptors, AMPA
  • Receptors, Kainic Acid
  • Receptors, Metabotropic Glutamate
  • Receptors, N-Methyl-D-Aspartate
  • metabotropic glutamate receptor 2
  • metabotropic glutamate receptor 3
  • metabotropic glutamate receptor 6
  • metabotropic glutamate receptor 7
  • Glutamic Acid
  • metabotropic glutamate receptor 4