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Selective mediation of nerve injury-induced tactile hypersensitivity by neuropeptide Y.
J Neurosci. 2002 Nov 15; 22(22):9858-67.JN

Abstract

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.

Authors+Show Affiliations

Department of Pharmacology, College of Medicine, University of Arizona, Tucson, Arizona 85724, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

12427842

Citation

Ossipov, Michael H., et al. "Selective Mediation of Nerve Injury-induced Tactile Hypersensitivity By Neuropeptide Y." The Journal of Neuroscience : the Official Journal of the Society for Neuroscience, vol. 22, no. 22, 2002, pp. 9858-67.
Ossipov MH, Zhang ET, Carvajal C, et al. Selective mediation of nerve injury-induced tactile hypersensitivity by neuropeptide Y. J Neurosci. 2002;22(22):9858-67.
Ossipov, M. H., Zhang, E. T., Carvajal, C., Gardell, L., Quirion, R., Dumont, Y., Lai, J., & Porreca, F. (2002). Selective mediation of nerve injury-induced tactile hypersensitivity by neuropeptide Y. The Journal of Neuroscience : the Official Journal of the Society for Neuroscience, 22(22), 9858-67.
Ossipov MH, et al. Selective Mediation of Nerve Injury-induced Tactile Hypersensitivity By Neuropeptide Y. J Neurosci. 2002 Nov 15;22(22):9858-67. PubMed PMID: 12427842.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Selective mediation of nerve injury-induced tactile hypersensitivity by neuropeptide Y. AU - Ossipov,Michael H, AU - Zhang,En-Tan, AU - Carvajal,Cristina, AU - Gardell,Luis, AU - Quirion,Remi, AU - Dumont,Yvan, AU - Lai,Josephine, AU - Porreca,Frank, PY - 2002/11/13/pubmed PY - 2002/11/26/medline PY - 2002/11/13/entrez SP - 9858 EP - 67 JF - The Journal of neuroscience : the official journal of the Society for Neuroscience JO - J Neurosci VL - 22 IS - 22 N2 - 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. SN - 1529-2401 UR - https://www.unboundmedicine.com/medline/citation/12427842/Selective_mediation_of_nerve_injury_induced_tactile_hypersensitivity_by_neuropeptide_Y_ L2 - http://www.jneurosci.org/cgi/pmidlookup?view=long&pmid=12427842 DB - PRIME DP - Unbound Medicine ER -