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. Author manuscript; available in PMC: 2014 Apr 15.
Published in final edited form as: J Immunol. 2013 Mar 13;190(8):3895–3904. doi: 10.4049/jimmunol.1203001

Figure 2. IFNγ-deficiency protects NOD.AireGW/+ mice from abnormalities associated with chronic demyelination on motor nerve electrophysiology.

Figure 2

A–C) Representative distal and proximal compound muscle action potentials from the sciatic nerve of age-matched wildtype (A), neuropathic IFNγ-sufficient NOD.AireGW/+ (B), and age-matched IFNγ-deficient NOD.AireGW/+ (C) mouse. D) Mean amplitude, conduction velocity, and duration of compound muscle action potentials from wildtype, neuropathic IFNγ-sufficient NOD.AireGW/+ and age-matched IFNγ-deficient NOD.AireGW/+ mice. * represents p<0.05. At least 3 mice were included in each group.