RT Journal Article
SR Electronic
T1 Reflex neurogenic inflammation. I. Contribution of the peripheral nervous system to spatially remote inflammatory responses that follow injury
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 1380
OP 1386
DO 10.1523/JNEUROSCI.05-05-01380.1985
VO 5
IS 5
A1 JD Levine
A1 SJ Dardick
A1 AI Basbaum
A1 E Scipio
YR 1985
UL http://www.jneurosci.org/content/5/5/1380.abstract
AB Recent studies of the mechanism of neurogenic inflammation have focused on the contribution of neuropeptides released from peripheral terminals of primary afferent sensory neurons. In this study we addressed the contribution of humoral and neural factors to the hyperalgesia and swelling that are produced contralateral to an injured hindpaw, a phenomenon which we refer to as reflex neurogenic inflammation. The contralateral inflammatory response develops gradually, over a period of hours, and shows no tachyphylaxis with repeated application of the same stimulus. Denervation of either limb significantly attenuated the contralateral responses. Selective lesions of small-diameter, presumed nociceptive afferent fibers with capsaicin, or of sympathetic postganglionic efferents by immunosympathectomy, also reduced swelling and hyperalgesia of the uninjured paw. Interruption of venous circulation to the injured limb by vein ligation did not alter the response in the contralateral paw. Taken together, these data suggest that reflex neurogenic inflammation is neurally mediated, via connections across the spinal cord.