| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
NEUROSCIENCE |
1 Department of Anesthesia, Critical Care and Pain Management, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA
Peripheral nerve inflammation can cause axons conducting through the inflamed site to become mechanically sensitive. Axonal mechanical sensitivity (AMS) of intact axons may explain symptoms in a diverse number of conditions characterized by radiating pain evoked by movements of the affected nerve. Because nerve inflammation also disrupts axoplasmic transport, we hypothesized that the disruption of axoplasmic transport by nerve inflammation could cause the cellular components responsible for mechanical transduction to accumulate and become inserted at the inflamed site, causing AMS. This was tested by examining AMS in C-fibre nociceptors following the application of axoplasmic transport blockers (colchicine and vinblastine) to the sciatic nerve. Both 10 mM colchicine and 0.1 mM vinblastine caused AMS to develop in 30.6% and 33.3% of intact axons, respectively (P < 0.05 compared to sham treatment). Since high doses of colchicine (> 50 mM) can damage axons, and inflammation is involved in the removal of axonal debris, experiments were performed to assess conduction across the treatment site as well as signs of inflammation. Results indicated minimal axonal loss (95% of A- and C-fibres conducting), consistent with the normal microscopic appearance of the colchicine treatment site and absence of ED1-positive (recruited) macrophages. In a separate series of experiments, the block of axoplasmic transport proximal to a localized neuritis significantly reduced inflammation-induced AMS (15.6% compared to 55.6%; P < 0.05), further supporting that the components necessary for AMS are moved by anterograde transport. In summary, nerve inflammation that causes the disruption of axoplasmic transport in patients with painful conditions may result in the accumulation and insertion of mechanosensitive elements at the inflamed site.
(Received 29 August 2007;
accepted after revision 15 November 2007;
first published online 15 November 2007)
Corresponding author A. Dilley: Division of Clinical and Laboratory Investigation, Brighton and Sussex Medical School, Medical School Building, University of Sussex, Falmer, Brighton BN1 9PX, UK. Email: a.dilley{at}bsms.ac.uk
This article has been cited by other articles:
|
|
 |
|
  T. Hoffmann, S. K. Sauer, R. E. Horch, and P. W. Reeh Sensory Transduction in Peripheral Nerve Axons Elicits Ectopic Action Potentials J. Neurosci., June 11, 2008; 28(24): 6281 - 6284. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. R. Mehta and A. R. Mehta How does inflammation affect axonal excitability to mechanical stimulation of neurones in the rat pain pathway? J. Physiol., May 1, 2008; 586(9): 2247 - 2248. [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
