Summary
Recently the K+ channel blocker 4-aminopyridine (4-AP) has been suggested to be useful to improve motor deficits due to spinal cord lesions. There is, however, little basic research support for this action of 4-AP. In this study we have used as a model the neonatal mammalian spinal cord in vitro that generates a rhythmic activity termed fictive locomotion (induced by bath-application of NMDA + 5-HT) with phasic electrical discharges alternating between flexor and extensor motor pools and between left and right motoneurons within the same segment. When 4-AP was added in the presence of sub-threshold concentrations of NMDA + 5-HT, there was facilitation of fictive locomotion which appeared with alternating patterns on all recorded ventral roots (VR). Furthermore, in the presence of 4-AP, weak dorsal root (DR) stimuli, previously insufficient to activate locomotor patterns, generated alternating discharges from various VRs. The present data show that 4-AP could strongly facilitate the locomotor program initiated by neurochemicals or electrical stimuli, indicating that the spinal locomotor network is a very sensitive target for the action of 4-AP.
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© 2005 Springer-Verlag
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Taccola, G., Nistri, A. (2005). Electrophysiological effects of 4-aminopyridine on fictive locomotor activity of the rat spinal cord in vitro. In: von Wild, K.R.H. (eds) Re-Engineering of the Damaged Brain and Spinal Cord. Acta Neurochirurgica Supplementum, vol 93. Springer, Vienna. https://doi.org/10.1007/3-211-27577-0_26
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DOI: https://doi.org/10.1007/3-211-27577-0_26
Publisher Name: Springer, Vienna
Print ISBN: 978-3-211-24150-9
Online ISBN: 978-3-211-27577-1
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