Up-regulation of neuropeptide Y levels and modulation of glutamate release through neuropeptide Y receptors in the hippocampus of kainate-induced epileptic rats

Details

Serval ID
serval:BIB_2CA5D14DF8A3
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Up-regulation of neuropeptide Y levels and modulation of glutamate release through neuropeptide Y receptors in the hippocampus of kainate-induced epileptic rats
Journal
Journal of Neurochemistry
Author(s)
Silva  A. P., Xapelli  S., Pinheiro  P. S., Ferreira  R., Lourenco  J., Cristovao  A., Grouzmann  E., Cavadas  C., Oliveira  C. R., Malva  J. O.
ISSN
0022-3042 (Print)
Publication state
Published
Issued date
04/2005
Volume
93
Number
1
Pages
163-70
Notes
Comparative Study
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Apr
Abstract
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.
Keywords
Animals Disease Models, Animal Drug Interactions Epilepsy/chemically induced/*metabolism Glutamic Acid/*metabolism Hippocampus/drug effects/*metabolism Kainic Acid Male Neuropeptide Y/*analogs & derivatives/genetics/*metabolism/pharmacology Peptide Fragments/pharmacology Potassium Chloride/pharmacology RNA, Messenger/biosynthesis Rats Rats, Wistar Receptors, Neuropeptide Y/antagonists & inhibitors/classification/*physiology Reverse Transcriptase Polymerase Chain Reaction/methods Time Factors Up-Regulation/drug effects/physiology
Pubmed
Web of science
Create date
25/01/2008 10:55
Last modification date
20/08/2019 13:11
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