Extended Data Fig. 2: DRG neurons are normal in Snx25+/− mice.
(a) Scheme of the targeting construct used to knock out the Snx25 gene. (b) Hot plate test of WT and Snx25+/− mice. Left panel shows latencies of 2-month-old mice (WT: n = 8; Snx25+/−: n = 16, p = 0.222). Right panel shows those of 6–8-month-old mice (WT: n = 11; Snx25+/−: n = 13, p = 0.006). s, second. (c) Size distribution of DRG neuron diameters is plotted for WT and Snx25+/− mice (L4 level, WT (blue columns): 814 cells from 3 mice; Snx25+/− mice (red columns): 709 cells from 3 mice). X-axis values indicate the maximum diameter in each 5-μm range (for example, 10 indicates diameters ranging from 5 μm to 10 μm). Numbers above or inside columns are the actual numbers of cells in each diameter range. Inset, cumulative frequency distribution of soma diameters. (d) Left, representative confocal microscopic images showing CGRP-immunoreactive neurons in the DRG (L4) of WT and Snx25+/− mice. Scale bar, 100 μm. Right, percentage of CGRP-positive cells among Nissl-positive cells in WT and Snx25+/− mice (WT: n = 7; Snx25+/−: n = 9 DRG sections from at least 3 different mice of each genotype, p = 0.521). (e) Left, representative confocal microscopic images of fluorescent Nissl-stained and NF200-immunoreactive neurons in the DRG (L4) of WT and Snx25+/− mice. Scale bar, 100 μm. Right, percentage of NF200-positive cells among Nissl-positive cells (WT: n = 3; Snx25+/−: n = 3 DRG sections from at least 3 different mice of each genotype, p = 0.903). Results are represented as mean ± SEM. Statistical analyses were performed using the two-tailed Student’s t-test. **p < 0.01. n.s., not significant. Representative of three independent experiments (d and e).
