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. 2018 Feb 12;12:5. doi: 10.3389/fnint.2018.00005

Figure 3.

Figure 3

Optical stimulation of ChR2+ bladder afferents potentiated bladder nociception. (A,B) Representative raw EMG traces from Trpv1Cre;Ai32 and Scn10aCre;Ai32 mice during 30 and 50 mmHg bladder distension before (baseline) and during (laser on) blue light illumination. (C) Transurethral fiber optic delivery of blue light to the bladder lumen (laser on) in Trpv1Cre;Ai32 mice significantly increased the evoked responses to bladder distension compared with pre-laser (baseline) responses (**P < 0.01, two-way ANOVA; n = 8 mice). Significant potentiation occurred at noxious distension pressures (30–50 mmHg, all P values <0.05). (D) Potentiation of the VMR was light intensity-dependent in Trpv1Cre;Ai32 mice (*P < 0.05, two-way ANOVA; n = 6 mice). (E) Optical stimulation of ChR2+ bladder afferents (laser on) significantly increased the evoked response to bladder distension compared with pre-laser (baseline) responses in Scn10aCre;Ai32 mice (*P < 0.05, two-way ANOVA; n = 8 mice). Distension-evoked responses were potentiated at both noxious (30–50 mmHg, *P values <0.05) and non-noxious (20 mmHg, *P < 0.05) pressures. (F) As in Trpv1Cre;Ai32 mice, potentiation of the VMR was light intensity-dependent in Scn10aCre;Ai32 mice (*P < 0.05, two-way ANOVA; n = 6 mice).