Journal
JOURNAL OF NEUROCHEMISTRY
Volume 93, Issue 1, Pages 163-170Publisher
WILEY-BLACKWELL
DOI: 10.1111/j.1471-4159.2004.03005.x
Keywords
epilepsy; glutamate; hippocampus; neuropeptide Y; synaptosomes
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Kainate-induced epilepsy has been shown to be associated with increased levels of neuropeptide Y (NPY) in the rat hippocampus. However, there is no information on how increased levels of this peptide might modulate excitation in kainate-induced epilepsy. In this work, we investigated the modulation of glutamate release by NPY receptors in hippocampal synaptosomes isolated from epileptic rats. In the acute phase of epilepsy, a transient decrease in the efficiency of NPY and selective NPY receptor agonists in inhibiting glutamate release was observed. Moreover, in the chronic epileptic hippocampus, a decrease in the efficiency of NPY and the Y-2 receptor agonist, NPY13-36, was also found. Simultaneously, we observed that the epileptic hippocampus expresses higher levels of NPY, which may account for an increased basal inhibition of glutamate release. Consistently, the blockade of Y-2 receptors increased KCl-evoked glutamate release, and there was an increase in Y-2 receptor mRNA levels 30 days after kainic acid injection, suggesting a basal effect of NPY through Y-2 receptors. Taken together, these results indicate that an increased function of the NPY modulatory system in the epileptic hippocampus may contribute to basal inhibition of glutamate release and control hyperexcitability.
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