Charcot-Marie-Tooth (CMT) disease is the most common hereditary peripheral neuropathy encompassing a group of heterogeneous disorders characterised by distal limb areflexia and muscle atrophy, high-arched feet (known clinically as pes cavus), and decreased axonal conduction velocities. At present, there is no effective drug therapy for CMT despite intensive investigation of the molecular genetics of the condition. Our laboratory has recently found that normal nerve striations (the “bands of Fontana”) appear to be absent on the surface of Trembler-J mouse nerves, an animal model of CMT type 1A, suggesting structural abnormalities in the underlying undulating course of component nerve fibres in an unstretched specimen. Previous studies have identified a correlation between peripheral nerve injury and the loss of observable striations on whole nerve fascicles (Zachary et al., 1993). In light of these findings, the current study investigated the hypothesis that the chronic progressive peripheral neuropathy of CMT1A is a result of disordered nerve biomechanics and increased susceptibility to stretch-induced axonal injury. Trembler-J (PMP22Tr-J/+; 21-27g; n=8) and wild-type C57BL/6 (PMP22+/+; 20-27g; n=8) mice were killed humanely by stunning and cervical dislocation in accordance with institutional guidelines. Sciatic nerves were isolated and examined using a sealed humidity chamber and stimulated electrically with simultaneous application of uniaxial tensile stresses. Young’s modulus of elasticity was derived from the slope of the stress-strain curve and used as a measure of the biomechanical properties of each nerve. Electrophysiological responses to nerve deformation were also recorded as a measure of the capacity of nerves to propagate electrical potentials. Results are presented as mean ± S.E.M. with a criterion for statistical significance set at p<0.05. Upon application of tensile force, a significant difference was observed between the change in compound action potential (CAP) peak amplitude per unit of change in percentage (%) strain in both groups; with control mice showing an average decline in CAP of -0.07 ± 0.03mV per unit % strain, while Trembler-J nerves showed an average increase of 0.02 ± 0.02mV (p=0.028, two-tailed Student’s t-test) despite no significant difference in Young’s moduli (p=0.5, Mann-Whitney U test). The findings lead to rejection of the original hypothesis and indicate that the peripheral nerves of Trembler-J mice are not more prone to stretch-induced failure of impulse conduction.