Figure 6
mIPSC alterations are independent of inhibitory synapse number.
Total inhibitory synapse density does not differ among Slc7a10 genotypes, as assessed by gephyrin (GPHN) density in the spinal cord ventral horn of P10-P12 mice (p = 1.0 for wild type vs. knockout; p = 1.0 for wild type vs. heterozygote; p = 0.9 for wild type vs. heterozygote) (a–d). n = 3 biological replicates for each genotype. Glycinergic synaptic architecture is grossly unaltered among Slc7a10 genotypes. Total spinal cord content of the glycine receptor (GLYR, e), GLYT1 (f), GLYT2 (g), and VIAAT (h) does not differ among wild type, heterozygous, and knockout animals. Beta-tubulin loading controls are shown below each blot (the same loading control was used for GLYR and GLYT2). n = 3 biological replicates for each genotype; p > 0.3 for all pairwise comparisons except for SLC7A10 (p < 0.02 for differences among genotypes). Full-length immunoblots are presented in Supplementary Figure S1. SLC7A10 deficiency does not cause loss of spinal cord glycinergic neurons. Glycinergic neuron density does not differ among genotypes, as assessed by count of GFP-positive cells in spinal cords of P10-P12 mice, in which GFP expression is directed by the promoter of the glycinergic neuronal marker GLYT2 (j–m) (p = 0.7 for wild type vs. knockout, p = 1.0 for wild type vs. heterozygote; p = 0.1 for heterozygote vs. knockout). n = 3 biological replicates for each genotype. Scale bar, 100 μm.
