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¹ Institute for Physiology and Pathophysiology, University of Erlangen-Nuremberg, Erlangen, Germany

Axonal conduction velocity varies according to the level of preceding impulse activity. In unmyelinated axons this typically results in a slowing of conduction velocity and a parallel increase in threshold. It is currently held that Na⁺–K⁺-ATPase-dependent axonal hyperpolarization is responsible for this slowing but this has long been equivocal. We therefore examined conduction velocity changes during repetitive activation of single unmyelinated axons innervating the rat cranial meninges. In direct contradiction to the currently accepted postulate, Na⁺–K⁺-ATPase blockade actually enhanced activity-induced conduction velocity slowing, while the degree of velocity slowing was curtailed in the presence of lidocaine (10–300 µM) and carbamazepine (30–500 µM) but not tetrodotoxin (TTX, 10–80 nM). This suggests that a change in the number of available sodium channels is the most prominent factor responsible for activity-induced changes in conduction velocity in unmyelinated axons. At moderate stimulus frequencies, axonal conduction velocity is determined by an interaction between residual sodium channel inactivation following each impulse and the retrieval of channels from inactivation by a concomitant Na⁺–K⁺-ATPase-mediated hyperpolarization. Since the process is primarily dependent upon sodium channel availability, tracking conduction velocity provides a means of accessing relative changes in the excitability of nociceptive neurons.

(Received 24 September 2007; accepted after revision 14 December 2007; first published online 20 December 2007)
Corresponding author R. W. Carr: Department of Physiology, University of Munich, Pettenkoferstrasse 12, D-80336 Munich, Germany. Email: richard.carr{at}med.uni-muenchen.de

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