(a) We measured motor neuron area at the L5 level of the lumbar spinal cord in sections from 13 month-old mice of the indicated genotype (n = 3 mice/genotype; 100–120 motor neurons/genotype). **P < .01, ***P < .001; ANOVA with post-hoc Bonferroni test.
(b) We quantified axon numbers, measuring diameters, in the L5 motor root for mice of the indicated genotype (n = 3 mice/genotype; 800 – 850 axons counted/individual mouse).
(c) Comparison of number of large caliber (> 9 μm diameter) motor axons from (b). *P < .05; ANOVA with post-hoc Bonferroni test. Error bars = s.e.m.
(d) Quantification of propidium iodide-positive primary cortical neurons from SETX-L389S+/− mice and littermate control mice (n = 3 mice/genotype; 9 technical replicates/individual mouse). **P < .01, t-test.
(e) We cultured primary cerebellar granule neurons (CGNs) from SETX-L389S+/− mice and littermate control mice in media containing 25 mM KCl, subjected the CGNs to potassium withdrawal by switching them to 5 mM KCl for either 6 hrs or 8 hrs, and then performed immunoblot analysis of CGN protein lysates for cleaved caspase-3. Beta-actin served as the loading control.
(f) Quantification of cleaved caspase-3 level normalized to beta-actin for CGNs subjected to potassium withdrawal for 8 hrs (n = 9 mice/genotype). *P < .05, t-test.
Error bars = s.e.m.