Abstract

BACKGROUND
Metabotropic glutamate receptors (mGluRs) participate in the induction of synaptic plasticity phenomena, such as long-term potentiation and long-term depression that are thought to be at the origin of learning and memory. They are also likely to play a role in modulating glutamate-induced neurotoxicity. It will become apparent that mGluRs are excellent targets for the development of drugs that modulate excitatory synaptic transmission. But there were several controversies about the exact role of group 1 mGluRs subtype 5 (mGluR5). This study was designed for evaluation of the neuroprotective role of mGluR5.
METHODS
Fifty male Sprague-Dawley rats were divided into three groups, control, MK-801 and lamotrigine. The hippocampus and basal ganglia were removed at 6 hours and 3 days after the one hour transient middle cerebral artery occlusion. The gene expression of mRNA of the brain samples were evaluated by using reverse transcriptase polymerase chain reaction technique.
RESULTS
The gene expression of mGluR5 mRNA in hippocampus was increased by 101.96 +/- 18.45% at 6 hours after ischemia and decreased by 50.70 +/- 15.73% at 3 days after ischemia (p<0.01). MK-801 and lamotrigine attenuated the ischemia-induced increases of gene expression of mGluR5 mRNA. In MK-801 group, the expression in basal ganglia was increased by only 0.23 +/- 5.41% at 6 hours after ischemia and decreased by 9.82 +/- 4.35% at 3 days after ischemia. In MK-801 group, the expression in hippocampus was decreased by 3.45 +/- 8.24% and 9.35 5.69% at 6 hours and 3 days after ischemia. In lamotrigine group, the expressions in hippocampus and basal ganglia were decreased by 26.66 +/- 9.85% and 9.45 +/- 5.22% at 6 hours after ischemia.
CONCLUSIONS
From these results, the role of mGluR5 was defined as a mediator for neuronal damage after transient focal cerebral ischemia in hippocampus and basal ganglia.

• Keywords: Focal brain ischemia;Lamotrigine;Metabotropic glutamate receptor subtype 5 (mGluR5);MK-801;RT-PCR;