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. Author manuscript; available in PMC: 2013 Oct 19.
Published in final edited form as: Nat Neurosci. 2007 Apr 15;10(5):615–622. doi: 10.1038/nn1876

Figure 3.

Figure 3

Marked toxicity of mutated SOD1–expressing astrocytes to motor neurons. (a,b) ESMNs show shorter axonal lengths (a) and smaller cell body diameters (b) when plated on AMLs expressing SOD1G93A, compared with their counterparts plated on NTgAMLs (Kolmogorov-Smirnov test; P < 0.005). (c) The decay in numbers of eGFPPMNs plated on G93AAMLs is greater (F3,37 = 6.3, P = 0.0015) than that of eGFPPMNs plated on NTgAMLs. (d) At 7 d after plating, there are consistently fewer eGFPPMNs (P < 0.01) in G93A, G37R and G85RAML cocultures than in NTgAML cocultures. However, WT and NTgAML cocultures have similar (P > 0.05) numbers of NTgPMNs. (e,f) ESMNs plated on either NTg or TgAMLs behave similarly to PMNs. (g) There are comparable numbers (P > 0.05) of NTg and G37RPMNs surviving at all time points after plating on NTgAMLs. There are fewer (*P < 0.01) NTg and G37RPMNs surviving on G93AAMLs than on NTgAMLs. The loss of G37RPMNs plated on G93AAMLs is comparable (P > 0.05) to that of NTgPMNs. Values represent means ± s.e.m. from at least three independent experiments performed at least in triplicate, analyzed by two-way ANOVA followed by a Newman-Keuls post hoc test. Tg, transgenic.