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Journal of Neuroscience, Vol 6, 3423-3429, Copyright © 1986 by Society for Neuroscience
Contribution of sensory afferents and sympathetic efferents to joint injury in experimental arthritis
JD Levine, SJ Dardick, MF Roizen, C Helms and AI Basbaum
We used pharmacological and surgical methods to determine the contribution
of several neural components to joint injury in rats with adjuvant-induced
arthritis. Both neonatal administration of capsaicin, which eliminates
small-diameter afferents, and peripheral sympathectomy, which depletes
catecholamines, attenuated joint injury. In contrast, the arthritis was
more severe in spontaneously hypertensive rats, which have increased
sympathetic tone. To address the contribution of the central vs peripheral
afferent terminal selectively, a group of rats underwent unilateral dorsal
rhizotomy. These rats developed a more severe arthritis in the deafferented
limb. The increase in arthritis severity produced by dorsal rhizotomy could
be reduced by prior sympathectomy or, less effectively, by prior treatment
with capsaicin. The latter observation suggests that large- diameter
afferents that are cut during dorsal rhizotomy also influence inflammation.
Finally, intracerebroventricular injection of morphine attenuated the
severity of arthritis, possibly through activation of bulbospinal
sympathoinhibitory circuits. Taken together, these data indicate that no
one class of nerve fiber is wholly responsible for the neurogenic component
of inflammation in experimental arthritis but that large- and
small-diameter afferents, sympathetic efferents, and CNS circuits that
modulate those fiber systems all influence the severity of joint injury in
arthritic rats.
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