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. 2014 Dec 12;9:56. doi: 10.1186/1750-1326-9-56

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© Rossi et al.; licensee BioMed Central. 2014

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Role of PKC/TRPV1 pathway in IL-1β-p53 interaction on glutamate synaptic transmission. A. Capsaicin, agonist of TRPV1 channels, caused a rapid and transient increase of sEPSC frequency in control conditions (p < 0.05) but not in slices pre-treated with PFT (p > 0.05). B. PKC activation with PMA was able to mimic IL-1β effects on sEPSC frequency in control slices, but not in presence of PFT. C. Nutlin, a p53 activator, enhances the IL-1β effects on sEPSC frequency (p < 0.05 respect to pre-drug value), but not in the presence of capsazepine (p > 0.05), TRPV1 channels antagonist, or chelerythrine (p > 0.05), PKC antagonist.