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The Journal of Neuroscience, November 15, 2002, 22(22):9858-9867

Selective Mediation of Nerve Injury-Induced Tactile Hypersensitivity by Neuropeptide Y

Michael H. Ossipov¹, En-Tan Zhang¹, Cristina Carvajal¹, Luis Gardell¹, Remi Quirion², Yvan Dumont², Josephine Lai¹, and Frank Porreca¹

¹ Department of Pharmacology, College of Medicine, University of Arizona, Tucson, Arizona 85724, and ² Douglas Hospital Research Centre, McGill University, Montreal, Quebec, Canada H4H 1R3

Prevention of nerve injury-induced tactile, but not thermal, hypersensitivity is achieved by ipsilateral lesions of the dorsal columns or lidocaine microinjection into the nucleus gracilis (n. gracilis). These and other data support the possibility that tactile hyperresponsiveness after nerve injury may be selectively mediated by a low-threshold myelinated fiber pathway to the n. gracilis. Here we identify a transmitter that might selectively mediate such injury-induced tactile hypersensitivity. Neuropeptide Y (NPY), normally not detected in the dorsal root ganglion (DRG) or in the n. gracilis of rats, became markedly upregulated at both sites and in the spinal cord after spinal nerve injury. Injury-induced NPY-IR occurred predominately in large-diameter DRG cells, and the NPY-IR in the n. gracilis was blocked by dorsal rhizotomy or dorsal column lesion. NPY microinjection into the n. gracilis of uninjured rats elicited reversible tactile, but not thermal, hypersensitivity only in the ipsilateral hindpaw. Administration of anti-NPY antiserum, but not control serum or preabsorbed serum, into the n. gracilis ipsilateral to nerve injury reversed tactile, but not thermal, hypersensitivity. Similarly, microinjection of the NPY antagonists NPY_18-36 and (R)-N-[[4-(aminocarbonylaminomethyl)-phenyl]methyl]-N2-(diphenylacetyl)-argininamide trifluoroacetate, into the n. gracilis ipsilateral to the injury reversed tactile, but not thermal, hypersensitivity. Antagonist administration into the contralateral n. gracilis had no effect on injury-induced hypersensitivity. These data suggest the selective mediation of nerve injury-induced tactile hypersensitivity by upregulated NPY via large fiber input to n. gracilis. Selective reversal of injury-induced tactile allodynia by NPY receptor antagonists would have significant implications for human neuropathic conditions.

Key words: neuropeptide Y; neuropathic pain; allodynia; nucleus gracilis; dorsal columns; dorsal column nuclei

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Copyright © 2002 Society for Neuroscience  0270-6474/02/22229858-10$05.00/0

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