Fig. 3.
Activation of protein kinase C γ is required for the expression of capsaicin-induced static–mechanical allodynia but not rubbing nociceptive behavior. (A) Bar histogram of the duration of the rubbing behavior in capsaicin-treated rats that have preemptively received intracisternal Tat carrier (50 pmol) alone or KIG31-1 (50 pmol) (n = 5 per group). The rubbing nociceptive behavior is not suppressed in KIG31-1-treated rats. (B) Time course of the changes in behavioral responses (allodynic score) evoked by static mechanical stimuli (6-g von Frey filament) applied 0.5 to 1 cm to the injection site, on the area of secondary hypersensitivity of the capsaicin-treated rats, preemptively treated with intracisternal KIG31-1 or Tat carrier alone (n = 5 per group). Static mechanical allodynia is completely suppressed in KIG31.1-treated rats. (C) Scatter plot of the number of extracellular signal–regulated kinase 1/2 phosphorylation (phospho-ERK1/2)-immunoreactive cells in laminae I-IIo, IIi-IIIo, and IIIi-V after 3-min static mechanical stimulation (6-g von Frey filament) applied on the area of secondary hypersensitivity, 30 min after capsaicin injection, in rats preemptively intracisternally injected with Tat carrier (500 pmol) or KIG31-1 (500 pmol) (n = 4 per group). Intracisternal KIG31-1 prevents stimulation-induced increase in the number of phospho-ERK1/2–immunoreactive cells in laminae I-IIo as well as IIi-IIIo in capsaicin-treated rats. Data are represented as the mean ± SD. *P < 0.05, ***P < 0.001.