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J Physiol Volume 560, Number 3, 807-819, November 1, 2004 DOI: 10.1113/jphysiol.2004.069443
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Mechanisms of hyperpolarization in regenerated mature motor axons in cat

Mihai Moldovan1 and Christian Krarup1

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

We found persistent abnormalities in the recovery of membrane excitability in long-term regenerated motor nerve fibres in the cat as indicated in the companion paper. These abnormalities could partly be explained by membrane hyperpolarization. To further investigate this possibility, we compared the changes in excitability in control nerves and long-term regenerated cat nerves (3–5 years after tibial nerve crush) during manoeuvres known to alter axonal membrane Na+–K+ pump function: polarization, cooling to 20°C, reperfusion after 10 min ischaemia, and up to 60 s of repetitive stimulation at 200 Hz. The abnormalities in excitability of regenerated nerves were reduced by depolarization and cooling and increased by hyperpolarization and during postischaemia. Moreover, the time course of recovery of excitability from repetitive stimulation and ischaemia was prolonged in regenerated nerves. Our data are consistent with an increased demand for electrogenic Na+–K+ pumping in regenerated nerves leading to membrane hyperpolarization. Such persistent hyperpolarization may influence the ability of the axon to compensate for changes in membrane potential following normal repetitive activity.

(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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M. Moldovan and C. Krarup
Persistent abnormalities of membrane excitability in regenerated mature motor axons in cat
J. Physiol., November 1, 2004; 560(3): 795 - 806.
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