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Intrathecal neuropeptide Y reduces behavioral and molecular markers of inflammatory or neuropathic pain.
Pain. 2008 Jul 15; 137(2):352-365.PAIN

Abstract

Our previous work indicates that the intrathecal administration of neuropeptide Y (NPY) acts at its cognate receptors to reduce behavioral signs of nociception in several models of inflammatory pain, including the formalin test. The present study extends these findings to a rat model of peripheral neuropathic pain, and then evaluates the hypothesis that NPY inhibits inflammation- and nerve injury-induced activation of spinal nociceptive transmission. Here we show that NPY dose-dependently reduced behavioral signs of mechanical and cold hypersensitivity in the spared nerve injury (SNI) model. Intrathecal administration of either a Y1 (BIBO3304) or a Y2 (BIIE0246) receptor antagonist dose-dependently reversed the anti-allodynic actions of NPY. To monitor the effects of NPY on the stimulus-induced activation of spinal nociresponsive neurons, we quantified protein expression of the immediate-early gene c-fos in lamina I-VI of the L4-L5 dorsal horn, with special attention to the mediolateral pattern of Fos immunohistochemical staining after SNI. Either tactile stimulation of the hindpaw ipsilateral to nerve injury, or intraplantar injection of noxious formalin, increased the number of Fos-like immunoreactive profiles. Tactile stimulation evoked a mediolateral pattern of Fos expression corresponding to the innervation territory of the uninjured (sural) nerve. We found that intrathecal NPY reduced both formalin- and SNI-induced Fos expression. NPY inhibition of SNI-induced Fos expression was localized to the sural (uninjured) innervation territory, and could be blocked by intrathecal BIBO3304 and BIIE0246. We conclude that NPY acts at spinal Y1 and Y2 receptors to reduce spinal neuron activity and behavioral signs of inflammatory or neuropathic pain.

Authors+Show Affiliations

Department of Pharmacology, School of Medicine, Tulane University Health Sciences Center, New Orleans, LA 70112, USA.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

17976913

Citation

Intondi, A B., et al. "Intrathecal Neuropeptide Y Reduces Behavioral and Molecular Markers of Inflammatory or Neuropathic Pain." Pain, vol. 137, no. 2, 2008, pp. 352-365.
Intondi AB, Dahlgren MN, Eilers MA, et al. Intrathecal neuropeptide Y reduces behavioral and molecular markers of inflammatory or neuropathic pain. Pain. 2008;137(2):352-365.
Intondi, A. B., Dahlgren, M. N., Eilers, M. A., & Taylor, B. K. (2008). Intrathecal neuropeptide Y reduces behavioral and molecular markers of inflammatory or neuropathic pain. Pain, 137(2), 352-365. https://doi.org/10.1016/j.pain.2007.09.016
Intondi AB, et al. Intrathecal Neuropeptide Y Reduces Behavioral and Molecular Markers of Inflammatory or Neuropathic Pain. Pain. 2008 Jul 15;137(2):352-365. PubMed PMID: 17976913.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Intrathecal neuropeptide Y reduces behavioral and molecular markers of inflammatory or neuropathic pain. AU - Intondi,A B, AU - Dahlgren,M N, AU - Eilers,M A, AU - Taylor,B K, Y1 - 2007/10/31/ PY - 2007/03/29/received PY - 2007/09/17/revised PY - 2007/09/19/accepted PY - 2007/11/3/pubmed PY - 2008/9/19/medline PY - 2007/11/3/entrez SP - 352 EP - 365 JF - Pain JO - Pain VL - 137 IS - 2 N2 - Our previous work indicates that the intrathecal administration of neuropeptide Y (NPY) acts at its cognate receptors to reduce behavioral signs of nociception in several models of inflammatory pain, including the formalin test. The present study extends these findings to a rat model of peripheral neuropathic pain, and then evaluates the hypothesis that NPY inhibits inflammation- and nerve injury-induced activation of spinal nociceptive transmission. Here we show that NPY dose-dependently reduced behavioral signs of mechanical and cold hypersensitivity in the spared nerve injury (SNI) model. Intrathecal administration of either a Y1 (BIBO3304) or a Y2 (BIIE0246) receptor antagonist dose-dependently reversed the anti-allodynic actions of NPY. To monitor the effects of NPY on the stimulus-induced activation of spinal nociresponsive neurons, we quantified protein expression of the immediate-early gene c-fos in lamina I-VI of the L4-L5 dorsal horn, with special attention to the mediolateral pattern of Fos immunohistochemical staining after SNI. Either tactile stimulation of the hindpaw ipsilateral to nerve injury, or intraplantar injection of noxious formalin, increased the number of Fos-like immunoreactive profiles. Tactile stimulation evoked a mediolateral pattern of Fos expression corresponding to the innervation territory of the uninjured (sural) nerve. We found that intrathecal NPY reduced both formalin- and SNI-induced Fos expression. NPY inhibition of SNI-induced Fos expression was localized to the sural (uninjured) innervation territory, and could be blocked by intrathecal BIBO3304 and BIIE0246. We conclude that NPY acts at spinal Y1 and Y2 receptors to reduce spinal neuron activity and behavioral signs of inflammatory or neuropathic pain. SN - 1872-6623 UR - https://www.unboundmedicine.com/medline/citation/17976913/Intrathecal_neuropeptide_Y_reduces_behavioral_and_molecular_markers_of_inflammatory_or_neuropathic_pain_ L2 - https://linkinghub.elsevier.com/retrieve/pii/00006396-200807150-00015 DB - PRIME DP - Unbound Medicine ER -