Fig. 4: TRPV1 is required for ocular cold nociception.
From: TRPV1 activity and substance P release are required for corneal cold nociception
a, b Although the reflex blinking response to cold was not altered in Trpv1−/− mice (n = 8), their eye closing responses were eliminated, compared with WT controls (n = 7). c The ocular width/length ratio of Trpv1−/− mice (n = 8) in response to cold (13 °C) was significantly greater than that of WT mice (n = 7), but lower than that of Trpm8−/− mice (n = 6). d The ocular width/length ratio in response to cold (13 °C) was increased in WT mice pre-treated with TRPV1 antagonist AMG9810 (0.2 nmol in 2 μL, 10 min before cold challenge; n = 5) compared with controls pre-treated with the vehicle (0.1% Tween-80 in saline; n = 5). e, f Representative images and group analysis show that TRPV1-deficiency did not impair the survival of corneal TRPM8-EGFPf neurons (retrogradely labeled by fluorogold from the cornea) in Trpv1−/−; Trpm8EGFPf/+ mice (n = 3), compared with control Trpv1+/+; Trpm8EGFPf/+ mice (n = 3). g Representative image showing that TRPM8-EGFPf sensory fibers (green) densely innervate the whole-mount cornea from Trpv1-/-; Trpm8EGFPf/+ mice. h Representative image showing the central projection of TRPM8-EGFPf fibers within the cornea-projection region in the spinal trigeminal nucleus of Trpv1−/−; Trpm8EGFPf/+ mice. Data are expressed as mean ± s.e.m. Statistical analysis by one-way ANOVA and two tailed Student’s t-test. n.s. not significant; *P < 0.05; **P < 0.01; ***P < 0.001. All images shown are representative of three independent experiments using tissues from at least three different mice. Scale bars in e, g, h 50, 100, and 250 μm, respectively. Source data are provided as a Source Data file.
