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. Author manuscript; available in PMC: 2018 Dec 1.
Published in final edited form as: Pain. 2017 Dec;158(12):2396–2409. doi: 10.1097/j.pain.0000000000001044

Figure 10. Neuronal sensitization during the progression of 4NQO-induced oral carcinogenesis.

Figure 10

Excitability was quantified with resting membrane potential (A), rheobase (B), and action potential (AP) threshold (C) in TG neurons from vehicle-treated mice (white bars, n = 5) and 4NQO-treated mice. Excitability parameters were analyzed across mice with similar histopathology: mild dysplasia (striped bars, n = 6) and severe (gray bars, n = 4) dysplasia, and oSCC (black bars, n = 5). One-way ANOVA analysis revealed significant differences between the 3 stages of cancer progression compared to neurons from vehicle-treated mice. Holm-Sidak post-hoc analysis showed significant differences between groups (as indicated, * p < 0.05, ** p < 0.01). D) A representative depolarization (4 milliseconds) evoked AP from a vehicle-treated (gray) and 4NQO-treated mouse with oSCC (black) in which we defined the active electrophysiological properties analyzed in Table 2. τ is time constant of AHP decay.