Fig 1: ES treatment with the presence of KCNN antagonist and agonist.A Representative images of IF labeling for β-III-tubulin (red) and GAP43 (green) in primary TG neurons under sham treatment, Apamin, in vitro ES, and ES combined with Apamin. B Quantification of the fluorescence intensity of GAP43, n = 4 for control group, n = 3 for the rest of the groups. C Corneal wholemount with β-III-tubulin staining of the corneal nerve in non-injured control, keratectomy injury with sham treatment, ES-treated injury, and ES-treated injury with Apamin groups. D Quantification of the total length of central 0.5 mm2 corneal plexus, n = 4. E, F Corneal sodium fluorescein staining image of non-DM control, STZ with sham treatment, ES-treated STZ, and ES-treated STZ with Apamin, and quantification, n = 8. G, H Corneal wholemount with β-III-tubulin immunolabeling in STZ model, and the total length of central 1 × 1 mm corneal plexus was quantified, n = 5 for the sham group, n = 8 for the rest of the groups. I, J Corneal images of sodium fluorescein staining taken from non-DM control, STZ with sham treatment, and KCNN agonist NS309-treated STZ groups, the NIH score is quantified, n = 4. K, L The corneal wholemount with β-III-tubulin and GAP43 staining are shown, and the average numbers of growth cones are provided, n = 4. All animals used are male. *p < 0.05; ** p < 0.01; *** p < 0.001; ****, p < 0.0001.