{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T13:40:00Z","timestamp":1792676400455,"version":"4.5.0"},"reference-count":60,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2008,2,18]],"date-time":"2008-02-18T00:00:00Z","timestamp":1203292800000},"content-version":"vor","delay-in-days":3,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2008,2,15]]},"abstract":"<jats:p>\n                    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\n                    <jats:sup>+<\/jats:sup>\n                    \u2013K\n                    <jats:sup>+<\/jats:sup>\n                    \u2010ATPase\u2010dependent 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\n                    <jats:sup>+<\/jats:sup>\n                    \u2013K\n                    <jats:sup>+<\/jats:sup>\n                    \u2010ATPase blockade actually enhanced activity\u2010induced conduction velocity slowing, while the degree of velocity slowing was curtailed in the presence of lidocaine (10\u2013300 \u03bc\n                    <jats:sc>m<\/jats:sc>\n                    ) and carbamazepine (30\u2013500 \u03bc\n                    <jats:sc>m<\/jats:sc>\n                    ) but not tetrodotoxin (TTX, 10\u201380 n\n                    <jats:sc>m<\/jats:sc>\n                    ). This suggests that a change in the number of available sodium channels is the most prominent factor responsible for activity\u2010induced 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\n                    <jats:sup>+<\/jats:sup>\n                    \u2013K\n                    <jats:sup>+<\/jats:sup>\n                    \u2010ATPase\u2010mediated 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.\n                  <\/jats:p>","DOI":"10.1113\/jphysiol.2007.145383","type":"journal-article","created":{"date-parts":[[2007,12,20]],"date-time":"2007-12-20T20:58:29Z","timestamp":1198184309000},"page":"1089-1103","source":"Crossref","is-referenced-by-count":142,"title":["Conduction velocity is regulated by sodium channel inactivation in unmyelinated axons innervating the rat cranial meninges"],"prefix":"10.1113","volume":"586","author":[{"given":"Roberto","family":"De Col","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karl","family":"Messlinger","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard 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