Contribution of sensory afferents and sympathetic efferents to joint injury in experimental arthritis.

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