Recent microneurographic evidence suggests that conduction velocity slowing profiles are altered in single axons from neuropathic patients ( Orstavik et al. For multi-unit microneurographic recordings of human unmyelinated C-fibres, activity-induced changes in conduction velocity also form the basis of the ‘marking’ technique employed to identify periods of activity in single unmyelinated axons. The slowing of axonal conduction velocity in response to activity can therefore be considered as an intrinsic means of self-inhibition in umyelinated axons.Īctivity-induced changes in conduction velocity are relatively homogeneous amongst sensory neurons of the same receptive sensory class and this index has therefore found use primarily in fibre classification ( Thalhammer et al. 1994), an increase in the minimum charge required for electrical activation ( Raymond, 1979) and the possibility of conduction failure ( Weidner et al. For neurons with unmyelinated axons, a considerable proportion of which are nociceptive, repetitive activation typically results in a progressive slowing of conduction velocity ( Thalhammer et al. The speed of action potential conduction in individual axons varies according to the level of preceding activity. 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. 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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