QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

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

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.
CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?

This article has been cited by other articles:

				P. M. Hermann, J. J. Nicol, A. G. M. Bulloch, and W. C. Wildering RGD-dependent mechanisms in the endoneurial phagocyte response and axonal regeneration in the nervous system of the snail Lymnaea stagnalis J. Exp. Biol., February 15, 2008; 211(4): 491 - 501. [Abstract] [Full Text] [PDF]

				R. M. S. Weragoda and E. T. Walters Serotonin Induces Memory-Like, Rapamycin-Sensitive Hyperexcitability in Sensory Axons of Aplysia That Contributes to Injury Responses J Neurophysiol, September 1, 2007; 98(3): 1231 - 1239. [Abstract] [Full Text] [PDF]

				Y.-J. Sung, E. T. Walters, and R. T. Ambron A Neuronal Isoform of Protein Kinase G Couples Mitogen-Activated Protein Kinase Nuclear Import to Axotomy-Induced Long-Term Hyperexcitability in Aplysia Sensory Neurons J. Neurosci., August 25, 2004; 24(34): 7583 - 7595. [Abstract] [Full Text] [PDF]

				L. R. Watkins and S. F. Maier Beyond Neurons: Evidence That Immune and Glial Cells Contribute to Pathological Pain States Physiol Rev, October 1, 2002; 82(4): 981 - 1011. [Abstract] [Full Text] [PDF]