![]() 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. 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. 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 μ m) and carbamazepine (30–500 μ m) but not tetrodotoxin (TTX, 10–80 n m). ![]() ![]() We therefore examined conduction velocity changes during repetitive activation of single unmyelinated axons innervating the rat cranial meninges. It is currently held that Na +–K +-ATPase-dependent axonal hyperpolarization is responsible for this slowing but this has long been equivocal. In unmyelinated axons this typically results in a slowing of conduction velocity and a parallel increase in threshold. Axonal conduction velocity varies according to the level of preceding impulse activity. ![]()
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