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This Article Full Text Full Text (PDF) All Versions of this Article: 560/3/795    most recent jphysiol.2004.069476v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Moldovan, M. Articles by Krarup, C. Search for Related Content PubMed PubMed Citation Articles by Moldovan, M. Articles by Krarup, C.

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

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.

(Received 4 June 2004; accepted after revision 2 August 2004; first published online 5 August 2004)
Corresponding author C. Krarup: Department of Clinical Neurophysiology NF3063, Rigshospitalet, 9 Blegdamsvej, 2100 Copenhagen, Denmark. Email: ckrarup{at}rh.dk

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