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Evidence that exogenous and endogenous fractalkine can induce spinal nociceptive facilitation in rats.
Eur J Neurosci. 2004 Nov; 20(9):2294-302.EJ

Abstract

Recent evidence suggests that spinal cord glia can contribute to enhanced nociceptive responses. However, the signals that cause glial activation are unknown. Fractalkine (CX3C ligand-1; CX3CL1) is a unique chemokine expressed on the extracellular surface of spinal neurons and spinal sensory afferents. In the dorsal spinal cord, fractalkine receptors are primarily expressed by microglia. As fractalkine can be released from neurons upon strong activation, it has previously been suggested to be a neuron-to-glial signal that induces glial activation. The present series of experiments provide an initial investigation of the spinal pain modulatory effects of fractalkine. Intrathecal fractalkine produced dose-dependent mechanical allodynia and thermal hyperalgesia. In addition, a single injection of fractalkine receptor antagonist (neutralizing antibody against rat CX3C receptor-1; CX3CR1) delayed the development of mechanical allodynia and/or thermal hyperalgesia in two neuropathic pain models: chronic constriction injury (CCI) and sciatic inflammatory neuropathy. Intriguingly, anti-CX3CR1 reduced nociceptive responses when administered 5-7 days after CCI, suggesting that prolonged release of fractalkine may contribute to the maintenance of neuropathic pain. Taken together, these initial investigations of spinal fractalkine effects suggest that exogenous and endogenous fractalkine are involved in spinal sensitization, including that induced by peripheral neuropathy.

Authors+Show Affiliations

Department of Psychology & the Center for Neuroscience, University of Colorado at Boulder, Boulder, CO 80309-0345, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo 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, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

15525271

Citation

Milligan, E D., et al. "Evidence That Exogenous and Endogenous Fractalkine Can Induce Spinal Nociceptive Facilitation in Rats." The European Journal of Neuroscience, vol. 20, no. 9, 2004, pp. 2294-302.
Milligan ED, Zapata V, Chacur M, et al. Evidence that exogenous and endogenous fractalkine can induce spinal nociceptive facilitation in rats. Eur J Neurosci. 2004;20(9):2294-302.
Milligan, E. D., Zapata, V., Chacur, M., Schoeniger, D., Biedenkapp, J., O'Connor, K. A., Verge, G. M., Chapman, G., Green, P., Foster, A. C., Naeve, G. S., Maier, S. F., & Watkins, L. R. (2004). Evidence that exogenous and endogenous fractalkine can induce spinal nociceptive facilitation in rats. The European Journal of Neuroscience, 20(9), 2294-302.
Milligan ED, et al. Evidence That Exogenous and Endogenous Fractalkine Can Induce Spinal Nociceptive Facilitation in Rats. Eur J Neurosci. 2004;20(9):2294-302. PubMed PMID: 15525271.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Evidence that exogenous and endogenous fractalkine can induce spinal nociceptive facilitation in rats. AU - Milligan,E D, AU - Zapata,V, AU - Chacur,M, AU - Schoeniger,D, AU - Biedenkapp,J, AU - O'Connor,K A, AU - Verge,G M, AU - Chapman,G, AU - Green,P, AU - Foster,A C, AU - Naeve,G S, AU - Maier,S F, AU - Watkins,L R, PY - 2004/11/5/pubmed PY - 2005/3/5/medline PY - 2004/11/5/entrez SP - 2294 EP - 302 JF - The European journal of neuroscience JO - Eur. J. Neurosci. VL - 20 IS - 9 N2 - Recent evidence suggests that spinal cord glia can contribute to enhanced nociceptive responses. However, the signals that cause glial activation are unknown. Fractalkine (CX3C ligand-1; CX3CL1) is a unique chemokine expressed on the extracellular surface of spinal neurons and spinal sensory afferents. In the dorsal spinal cord, fractalkine receptors are primarily expressed by microglia. As fractalkine can be released from neurons upon strong activation, it has previously been suggested to be a neuron-to-glial signal that induces glial activation. The present series of experiments provide an initial investigation of the spinal pain modulatory effects of fractalkine. Intrathecal fractalkine produced dose-dependent mechanical allodynia and thermal hyperalgesia. In addition, a single injection of fractalkine receptor antagonist (neutralizing antibody against rat CX3C receptor-1; CX3CR1) delayed the development of mechanical allodynia and/or thermal hyperalgesia in two neuropathic pain models: chronic constriction injury (CCI) and sciatic inflammatory neuropathy. Intriguingly, anti-CX3CR1 reduced nociceptive responses when administered 5-7 days after CCI, suggesting that prolonged release of fractalkine may contribute to the maintenance of neuropathic pain. Taken together, these initial investigations of spinal fractalkine effects suggest that exogenous and endogenous fractalkine are involved in spinal sensitization, including that induced by peripheral neuropathy. SN - 0953-816X UR - https://www.unboundmedicine.com/medline/citation/15525271/Evidence_that_exogenous_and_endogenous_fractalkine_can_induce_spinal_nociceptive_facilitation_in_rats_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0953-816X&date=2004&volume=20&issue=9&spage=2294 DB - PRIME DP - Unbound Medicine ER -