Ana P. Silva and Sara Xapelli contributed equally to this study.
Up-regulation of neuropeptide Y levels and modulation of glutamate release through neuropeptide Y receptors in the hippocampus of kainate-induced epileptic rats
Article first published online: 17 FEB 2005
Journal of Neurochemistry
Volume 93, Issue 1, pages 163–170, April 2005
How to Cite
Silva, A. P., Xapelli, S., Pinheiro, P. S., Ferreira, R., Lourenço, J., Cristóvão, A., Grouzmann, E., Cavadas, C., Oliveira, C. R. and Malva, J. O. (2005), Up-regulation of neuropeptide Y levels and modulation of glutamate release through neuropeptide Y receptors in the hippocampus of kainate-induced epileptic rats. Journal of Neurochemistry, 93: 163–170. doi: 10.1111/j.1471-4159.2004.03005.x
- Issue published online: 17 FEB 2005
- Article first published online: 17 FEB 2005
- Received October 12, 2004; revised manuscript received November 24, 2004; accepted November 24, 2004.
- neuropeptide Y;
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 Y2 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 Y2 receptors increased KCl-evoked glutamate release, and there was an increase in Y2 receptor mRNA levels 30 days after kainic acid injection, suggesting a basal effect of NPY through Y2 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.