Fig. 4: En1 positive neuron reduction from postnatal day 63 in the SOD1G93A mouse. | Nature Communications

Fig. 4: En1 positive neuron reduction from postnatal day 63 in the SOD1G93A mouse.

From: Locomotor deficits in a mouse model of ALS are paralleled by loss of V1-interneuron connections onto fast motor neurons

Fig. 4

a Microphotograph of a wild-type mouse hemicord after RNAscope in situ hybridization at postnatal day 63. Chat in green, En1 in orange and DAPI in blue. b Magnification of Chat and En1 expression in control conditions and c at P63 in a SOD1G93A mouse. d Quantifications of En1 positive neurons in control conditions versus postnatal day 45, 63, and 84 in the ALS mouse model. There was a reduction at P63 to about 75% and to about 68% at P84 compared to age-matching wild-types (one-way ANOVA and Dunnett’s post hoc, F(3, 14) = 13.45, P45 P = 0.3108, P63 P = 0.0010, P84 P = 0.0003; wt N =9, SOD1G93A N = 3 mice per timepoint). e Intensity-measurements of En1 positive dots present within the quantified neurons showed no differences among the different timepoints, indicating that En1 neurons still present in the SOD1G93A mouse do not show lower transcript expression at these than earlier timepoints (two-way ANOVA and Tukey’s multiple comparisons test, F(2, 12) = 0.02754, P45 P = 0.9990, P63 P = 0.9998, P84 P = 1; N = 3 independent mice per condition per timepoint). Scale bar in (a) =200 μm, scale bar in (c) =50 μm representative also for (b). A minimum of 60 pictures (as shown in (bc)) was quantified per condition. In all graphs, data are presented as mean values ± SEM. Source data are provided as a Source Data file.

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