PKC-Dependent Signaling Pathways within PAG and Thalamus Contribute to the Nitric Oxide-Induced Nociceptive Behavior

Figure 5

Activation of a PKC-independent and a PKC-mediated pathway by NO donors. (a) SNP-induced increase of IL-1β within PAG and thalamus (THAL) was unmodified by pretreatment with the calphostin C and prevented by aspirin (ASA). (b) The reduction of Iκ-Bα was partially prevented by calphostin C and completely restored by ASA. Calphostin C antagonized the downregulation of CREB (c) and prevented the increased expression of pCREB (d) and pSTAT1 (e). ^∗𝑃<0.05,^∗∗𝑃<0.01,^∗∗∗𝑃<0.001 compared with vehicle-treated control group; ^∘𝑃<0.05,^∘∘𝑃<0.01 compared with SNP-treated group.

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