Down-Regulation of AMPA Receptor Subunit GluR2 in Amygdaloid Kindling
Article first published online: 23 NOV 2002
Journal of Neurochemistry
Volume 64, Issue 1, pages 462–465, January 1995
How to Cite
Prince, H. K., Conn, P. J., Blackstone, C. D., Huganir, R. L. and Levey, A. I. (1995), Down-Regulation of AMPA Receptor Subunit GluR2 in Amygdaloid Kindling. Journal of Neurochemistry, 64: 462–465. doi: 10.1046/j.1471-4159.1995.64010462.x
- Issue published online: 23 NOV 2002
- Article first published online: 23 NOV 2002
- Received September 16, 1994; accepted October 13, 1994.
- Glutamate receptors;
- Piriform cortex
Abstract: Alterations in glutamatergic transmission are postulated to be important in kindling and epilepsy. The levels of α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor subunits (GluR1, 2, and 4) were compared in amygdalakindled and sham-operated animals using subunit-specific antibodies and quantitative western blotting. Four limbic regions were examined: limbic forebrain, piriform cortex/amygdala, hippocampus, and entorhinal cortex. When subunit levels were examined 24 h after the last stage 5 seizure, levels of GluR2 were found to be selectively reduced in limbic forebrain (30%) and piriform cortex/amygdala (25%), with no changes in other regions examined. In addition, no changes in the other subunits were observed in any region. The decrease in GluR2 that was observed in kindled animals at 24 h was no longer present at 1 week and 1 month after the last stage 5 seizure. Because the GluR2 subunit uniquely determines the calcium permeability of these receptors and because the piriform cortex has been implicated as a source of excitatory drive for limbic seizures, reduced GluR2 expression may be important in increasing neuronal excitability in kindling-induced epilepsy, or may reflect a compensatory mechanism resulting from kindling.