Persistent abnormalities of membrane excitability in regenerated mature motor axons in cat

Authors

  • Mihai Moldovan,

    1. Division of  Neurophysiology, Institute of  Medical Physiology, Panum Institute and the Department of  Clinical Neurophysiology, the Neuroscience Center, Rigshospitalet, University of  Copenhagen Copenhagen, Denmark
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  • Christian Krarup

    1. Division of  Neurophysiology, Institute of  Medical Physiology, Panum Institute and the Department of  Clinical Neurophysiology, the Neuroscience Center, Rigshospitalet, University of  Copenhagen Copenhagen, Denmark
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Corresponding author C. Krarup: Department of Clinical Neurophysiology NF3063, Rigshospitalet, 9 Blegdamsvej, 2100 Copenhagen, Denmark. Email: ckrarup@rh.dk

Abstract

The purpose of our study was to assess by threshold tracking internodal and nodal membrane excitability during the maturation process after tibial nerve crush in cat. Various excitability indices (EI) were computed non-invasively by comparing the threshold of a submaximal compound motor potential at different stimulation durations (strength–duration relationship), after a conditioning nerve impulse (recovery of excitability), or during the application of a polarizing current (threshold electrotonus). Four months after the lesion, regenerated nerves showed a higher rheobase, shorter chronaxie, shorter refractory period and higher than normal threshold variations during threshold electrotonus (TE). A partial recovery was observed during the first 2 years of maturation. The recovery to depolarizing TE seemed complete but all other EI remained abnormal even after 5 years of regeneration, the most pronounced being the 157 ± 8% (mean ±S.E.M.) increase in threshold during hyperpolarizing TE compared with 94 ± 4% in controls. These EI abnormalities are consistent with increased input impedance. Nevertheless, the time course of maturation and incomplete recovery of EI could only be partially explained by changes in fibre morphology. The highly abnormal response to hyperpolarizing but not to depolarizing TE suggests that voltage-dependent membrane function also remained abnormal, possibly due to membrane hyperpolarization.

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