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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 p53-IL-1β interaction on glutamate synaptic transmission. A. The graph shows that application of IL-1β, in mice brain slices, significantly enhanced sEPSC frequency (p < 0.05 respect to pre-drug values), an effect fully prevented by both IL-1ra and the p53 inhibitor PFT (p < 0.05 respect to pre-drug values). The electrophysiological traces on the right are examples of sEPSCs recorded from single striatal neurons, before and during the application of IL-1β, in control conditions and in slices pre-treated with PFT. B. PFT failed to affect TNF-α effects on sEPSC duration (p > 0.05). The electrophysiological traces on the right are examples of sEPSC mean peak, obtained by group analysis and recorded from striatal neurons in the presence of TNF-α and PFT. *means p < 0.05.