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Activation of the spinal cord complement cascade might contribute to mechanical allodynia induced by three animal models of spinal sensitization.
J Pain. 2005 Mar; 6(3):174-83.JP

Abstract

The present series of experiments examined whether the complement cascade might play a key role in the expression of mechanical allodynia. Soluble complement receptor 1 (sCR1) was used to block the activation of the membrane attack pathway of the complement cascade. In doing so, sCR1 prevents the formation of the biologically active end products C3a, C5a, and membrane attack complexes (MACs). Intrathecal sCR1 had no effect on the behavioral responses of control groups. In contrast, blockade of this pathway abolished the expression of mechanical allodynia induced by peripheral nerve inflammation (sciatic inflammatory neuropathy model), partial sciatic nerve injury (chronic constriction injury model), and intrathecal injection of human immunodeficiency virus type 1 gp120, a viral envelope protein that activates glia. The fact that enhanced nociception was prevented or reversed in all 3 paradigms suggests that complement might be broadly involved in spinally mediated pain enhancement. The mechanisms whereby complement activation might potentially affect the functioning of microglia, astrocytes, and neurons are discussed. The complement cascade has not been previously implicated in spinal sensitization. These data suggest that complement activation within the spinal cord might contribute to enhanced pain states and provide additional evidence for immune regulation of pain transmission.

Authors+Show Affiliations

Department of Psychology and the Center of Neuroscience, University of Colorado at Boulder, 80309, 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

Language

eng

PubMed ID

15772911

Citation

Twining, Carin M., et al. "Activation of the Spinal Cord Complement Cascade Might Contribute to Mechanical Allodynia Induced By Three Animal Models of Spinal Sensitization." The Journal of Pain, vol. 6, no. 3, 2005, pp. 174-83.
Twining CM, Sloane EM, Schoeniger DK, et al. Activation of the spinal cord complement cascade might contribute to mechanical allodynia induced by three animal models of spinal sensitization. J Pain. 2005;6(3):174-83.
Twining, C. M., Sloane, E. M., Schoeniger, D. K., Milligan, E. D., Martin, D., Marsh, H., Maier, S. F., & Watkins, L. R. (2005). Activation of the spinal cord complement cascade might contribute to mechanical allodynia induced by three animal models of spinal sensitization. The Journal of Pain, 6(3), 174-83.
Twining CM, et al. Activation of the Spinal Cord Complement Cascade Might Contribute to Mechanical Allodynia Induced By Three Animal Models of Spinal Sensitization. J Pain. 2005;6(3):174-83. PubMed PMID: 15772911.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Activation of the spinal cord complement cascade might contribute to mechanical allodynia induced by three animal models of spinal sensitization. AU - Twining,Carin M, AU - Sloane,Evan M, AU - Schoeniger,Diana K, AU - Milligan,Erin D, AU - Martin,David, AU - Marsh,Henry, AU - Maier,Steven F, AU - Watkins,Linda R, PY - 2005/3/18/pubmed PY - 2005/6/18/medline PY - 2005/3/18/entrez SP - 174 EP - 83 JF - The journal of pain JO - J Pain VL - 6 IS - 3 N2 - The present series of experiments examined whether the complement cascade might play a key role in the expression of mechanical allodynia. Soluble complement receptor 1 (sCR1) was used to block the activation of the membrane attack pathway of the complement cascade. In doing so, sCR1 prevents the formation of the biologically active end products C3a, C5a, and membrane attack complexes (MACs). Intrathecal sCR1 had no effect on the behavioral responses of control groups. In contrast, blockade of this pathway abolished the expression of mechanical allodynia induced by peripheral nerve inflammation (sciatic inflammatory neuropathy model), partial sciatic nerve injury (chronic constriction injury model), and intrathecal injection of human immunodeficiency virus type 1 gp120, a viral envelope protein that activates glia. The fact that enhanced nociception was prevented or reversed in all 3 paradigms suggests that complement might be broadly involved in spinally mediated pain enhancement. The mechanisms whereby complement activation might potentially affect the functioning of microglia, astrocytes, and neurons are discussed. The complement cascade has not been previously implicated in spinal sensitization. These data suggest that complement activation within the spinal cord might contribute to enhanced pain states and provide additional evidence for immune regulation of pain transmission. SN - 1526-5900 UR - https://www.unboundmedicine.com/medline/citation/15772911/Activation_of_the_spinal_cord_complement_cascade_might_contribute_to_mechanical_allodynia_induced_by_three_animal_models_of_spinal_sensitization_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1526590004011216 DB - PRIME DP - Unbound Medicine ER -