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Figure 2 | Molecular Neurodegeneration

Figure 2

From: Interleukin-1β causes excitotoxic neurodegeneration and multiple sclerosis disease progression by activating the apoptotic protein p53

Figure 2

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.

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