Data for research paper: The time course of ongoing activity during neuritis and following axonal transport disruption

<b>Data for paper appearing in 'Journal of Neurophysiology'</b><br><br>C- and A- fibre electrophysiology time course data following
neuritis and vinblastine-induced axonal transport disruption. Data set includes conduction velocities, ongoing activity
and axonal mechanical sensitivity data.<br><br><b>Abstract from research paper:</b><br>Local nerve inflammation
(neuritis) leads to ongoing activity and axonal mechanical sensitivity (AMS)
along intact nociceptor axons, and disrupts axonal transport. This
phenomenon forms the most feasible cause of radiating pain, such as
sciatica. We have previously shown that axonal transport disruption
without inflammation or degeneration also leads to AMS, but does not cause
ongoing activity at the time point when AMS occurs, despite causing cutaneous
hypersensitivity. However, there have been no systematic studies of ongoing
activity during neuritis or non-inflammatory axonal transport disruption. In
this study, we present the time course of ongoing activity from primary sensory
neurons following neuritis and vinblastine-induced axonal transport disruption.
Whereas 24% of C/slow Aδ-fiber neurons had ongoing activity during neuritis,
few (&lt;10%) A- and C-fiber neurons showed ongoing activity 1-15 days
following vinblastine treatment. In contrast, AMS increased transiently at
the vinblastine treatment site, peaking on day 4-5 (28% of C/slow Aδ-fiber
neurons) and resolved by day 15. Conduction velocities were slowed in all
groups. In summary, the disruption of axonal transport without
inflammation does not lead to ongoing activity in sensory neurons, including
nociceptors, but does cause a rapid and transient development of AMS. Since it
is proposed that AMS underlies mechanically-induced radiating pain, and a
transient disruption of axonal transport (as previously reported) leads to transient
AMS, it follows that processes that disrupt axonal transport, such as neuritis,
must persist to maintain AMS and the associated symptoms.

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