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The aim of this work was to identify changes in the signaling mechanisms associated with neuropeptide Y (NPY)\u2010mediated inhibition of glutamate release that may contribute to hyperexcitabil\u2010ity. Using isolated rat hippocampal nerve terminals, we showed that the KCl\u2010evoked glutamate release is inhibited by NPY Y\n                    <jats:sub>2<\/jats:sub>\n                    receptor activation and is potentiated by the stimulation of protein kinase C (PKC). Moreover, we observed that immediately after status epilepticus (6 h postinjection with kainate, 10 mg\/kg), the functional inhibition of glutamate release by NPY Y\n                    <jats:sub>2<\/jats:sub>\n                    receptors was transiently blocked concomitantly with PKC hyperacti\u2010vation. The pharmacological blockade of seizure\u2010activated PKC revealed again the Y\n                    <jats:sub>2<\/jats:sub>\n                    receptor\u2010mediated inhibition of glutamate release. The functional activity of PKC immediately after status epilepticus was as\u2010sessed by evaluating phosphorylation of the AMPA receptor subunit GluRl (Ser\u2010831), a substrate for PKC. Moreover, NPY\u2010stimulated [\n                    <jats:sup>35<\/jats:sup>\n                    S]GTP\u03b3S autoradiographic binding studies indicated that the common target for Y\n                    <jats:sub>2<\/jats:sub>\n                    receptor and PKC on the inhibition\/ potentiation of glutamate release was located downstream of the Y\n                    <jats:sub>2<\/jats:sub>\n                    receptor, or its interacting G\u2010protein, and involves voltage\u2010gated calcium channels.\u2014Silva, A. P., Lourenco, J., Xapelli, S., Ferreira, R., Kristiansen, H., Woldbye, D. P. D., Oliveira, C. R., Malva, J. O. Protein kinase C activity blocks neuropeptide Y\u2010mediated inhibition of glutamate release and contributes to excitability of the hippocampus in status epilepticus.\n                    <jats:italic>FASEB J.<\/jats:italic>\n                    21, 671\u2013681 (2007)\n                  <\/jats:p>","DOI":"10.1096\/fj.06-6163com","type":"journal-article","created":{"date-parts":[[2006,12,13]],"date-time":"2006-12-13T21:56:53Z","timestamp":1166047013000},"page":"671-681","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":38,"title":["Protein kinase C activity blocks neuropeptide Y\u2010mediated inhibition of glutamate release and contributes to excitability of the hippocampus in status epilepticus"],"prefix":"10.1096","volume":"21","author":[{"given":"Ana P.","family":"Silva","sequence":"first","affiliation":[{"name":"Institute of Pharmacology and Therapeutics Faculty of Medicine University of Coimbra Coimbra Portugal"},{"name":"Center for Neuroscience and Cell Biology University of Coimbra Coimbra Portugal"}]},{"given":"Joana","family":"Lourenco","sequence":"additional","affiliation":[{"name":"Center for Neuroscience and Cell Biology University of Coimbra Coimbra Portugal"}]},{"given":"Sara","family":"Xapelli","sequence":"additional","affiliation":[{"name":"Center for Neuroscience and Cell Biology University of Coimbra Coimbra Portugal"}]},{"given":"Raquel","family":"Ferreira","sequence":"additional","affiliation":[{"name":"Center for Neuroscience and Cell Biology University of Coimbra Coimbra Portugal"}]},{"given":"Heidi","family":"Kristiansen","sequence":"additional","affiliation":[{"name":"Laboratory of Neuropsychiatry Rigshospitalet University Hospital and Department of Pharmacology University of Copenhagen Denmark"}]},{"given":"David P. 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