spacer gif spacer gif spacer gif spacer gif spacer gif
QUICK SEARCH:   [advanced]


spacer gif
     Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents    

This Article
Right arrow Full Text (PDF)
Right arrow References
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Clatworthy, A. L.
Right arrow Articles by Grose, E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Clatworthy, A. L.
Right arrow Articles by Grose, E.

Journal of Experimental Biology, Vol 202, Issue 5 623-630, Copyright © 1999 by Company of Biologists

JOURNAL ARTICLES

Immune-mediated alterations in nociceptive sensory function in Aplysia californica

AL Clatworthy and E Grose
University of North Carolina at Charlotte, Department of Biology, Charlotte, NC 28223, USA. aclatwor@email.uncc.edu

Nerve injury in Aplysia californica is accompanied by a profound long-lasting enhancement of the excitability of nociceptive sensory neurons that have axons in injured nerves. It is likely that a variety of signals are involved in triggering this injury-induced sensory plasticity. The objective of the present study was to determine whether cells of the cellular defense system (hemocytes) play a role in the modulation of sensory excitability following injury. In support of such an idea, we have shown previously that the induction of a cellular defense reaction close to sensory axons is accompanied by an increase in the excitability of sensory neurons with axons close to responding hemocytes. Furthermore, in the present study, we verified that, following axonal crush, numerous hemocytes accumulate at the injured site on the nerve. Using a hemocyte/nervous system co-culture preparation, we found that there were no significant differences in the expression of injury-induced sensory plasticity between sensory neurons incubated in the presence or absence of hemocytes. To overcome some potential limitations of our co-culture preparation, we used the endotoxin lipopolysaccharide (LPS) as a tool to activate the hemocytes. Sensory cells incubated in the presence of LPS and hemocytes were significantly more excitable than sensory cells incubated in the presence of LPS alone. We speculate that the addition of LPS to the incubation medium containing hemocytes enhanced the release of hemocyte-derived cytokine-like factors such as interleukin-1 and tumor necrosis factor. These cytokine-like factors may act as signals to modulate the expression of injury-induced sensory hyperexcitability.




© The Company of Biologists Ltd 1999