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. Author manuscript; available in PMC: 2024 Jul 1.
Published in final edited form as: Nat Neurosci. 2023 Nov 23;27(1):34–47. doi: 10.1038/s41593-023-01496-0

Figure 1: ASO-mediated transient stathmin-2 suppression reduces nerve conduction velocity and triggers muscle denervation.

Figure 1:

(a) Schematic representation of intraventricular (ICV) administration of control or Stmn2 targeting ASOs (ASO1 and ASO2) in 3-month-old wild-type mice. Figure created using Biorender. (b) Quantification of Stmn2 mRNA levels by qRT-PCR 2 weeks after ICV injection. Statistical analysis by two-sided, one-way ANOVA with Dunnett’s multiple comparison test. P = 0.0004 for both pairs. (c) Immunoblot showing stathmin-2 protein levels in mice spinal cord extracts 8 weeks after the ICV injection. Heat shock protein 90 (HSP-90) was used as a loading control. Each lane was loaded with protein extracted from a different animal. (d) Nerve conduction velocity measurement in mice hindlimbs 8 weeks after ICV injection of ASOs. Statistical analysis by two-sided, one-way ANOVA Tukey’s multiple comparisons test. N=12 animals per condition. P < 0.0001 for both pairs. (e-f) Representative confocal images (e) and innervation rate quantification (f) of neuromuscular junctions (NMJs) in the gastrocnemius muscle 8 weeks after delivery of non-targeting or Stmn2 targeting ASOs. At least n=3 animals and 250 NMJs were analyzed per condition. Statistical analysis by two-sided, two-way ANOVA followed by Sidak’s multiple comparisons test. Fully innervated P <0.0001; partially innervated P = 0.0012; denervated P = 0.0144. All panels: Data points represent individual mice. Error bars plotted as SEM. ****, p <0.0001; ***, p < 0.001; **, p < 0.01; *, p <0.05; ns, p>0.05.