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Development of tactile allodynia and thermal hyperalgesia by intrathecally administered platelet-activating factor in mice.
Pain. 2004 Oct; 111(3):351-9.PAIN

Abstract

Platelet-activating factor (PAF) is a potent inflammatory lipid mediator in peripheral tissues. However, its role in mediation of nociception in central nervous system is unknown. In the present study, whether PAF plays some role in pain transduction in the spinal cord was studied in mice. Intrathecal injection of PAF induced tactile pain, tactile allodynia at as low as 10 fg to 1 pg with a peak response at 100 fg, while lyso-PAF was without effect in the range of doses. Tactile allodynia induced by PAF was blocked by a PAF receptor antagonists, TCV-309, WEB 2086 and BN 50739. The expression of PAF receptor mRNA by RT-PCR was observed in DRG and spinal cord in mice. ATP P2X receptor antagonists, pyridoxalphosphate-6-azophenyl-2',4'-disulfonic acid and 2',3'-O-(2,4,6-trinitrophenyl)adenosine 5-triphosphate, NMDA receptor antagonist, MK 801 and nitric oxide synthetase inhibitor, 7-nitroindazole blocked the PAF-induced tactile allodynia. PAF-induced tactile allodynia and thermal hyperalgesia disappeared in neonatally capsaicin-treated adult mice, while tactile allodynia but not thermal hyperalgesia induced by intrathecally injected alpha,beta-methylene ATP, a P2X receptor agonist, was capsaicin-insensitive. The present study demonstrated that PAF is a potent inducer of tactile allodynia and thermal hyperalgesia at the level of the spinal cord. PAF-evoked tactile allodynia is suggested to be mediated by ATP and the following NMDA and NO cascade through capsaicin-sensitive fiber, different from exogenously injected alpha,beta-methylene ATP which is insensitive to capsaicin treatment.

Authors+Show Affiliations

Department of Dental Pharmacology, Division of Integrated Medical Science, Hiroshima University Graduate School of Biomedical Sciences, Kasumi 1-2-3, Minami-ku, Hiroshima 734-8553, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

15363879

Citation

Morita, Katsuya, et al. "Development of Tactile Allodynia and Thermal Hyperalgesia By Intrathecally Administered Platelet-activating Factor in Mice." Pain, vol. 111, no. 3, 2004, pp. 351-9.
Morita K, Morioka N, Abdin J, et al. Development of tactile allodynia and thermal hyperalgesia by intrathecally administered platelet-activating factor in mice. Pain. 2004;111(3):351-9.
Morita, K., Morioka, N., Abdin, J., Kitayama, S., Nakata, Y., & Dohi, T. (2004). Development of tactile allodynia and thermal hyperalgesia by intrathecally administered platelet-activating factor in mice. Pain, 111(3), 351-9.
Morita K, et al. Development of Tactile Allodynia and Thermal Hyperalgesia By Intrathecally Administered Platelet-activating Factor in Mice. Pain. 2004;111(3):351-9. PubMed PMID: 15363879.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Development of tactile allodynia and thermal hyperalgesia by intrathecally administered platelet-activating factor in mice. AU - Morita,Katsuya, AU - Morioka,Norimitsu, AU - Abdin,Joynal, AU - Kitayama,Shigeo, AU - Nakata,Yoshihiro, AU - Dohi,Toshihiro, PY - 2003/12/17/received PY - 2004/05/24/revised PY - 2004/07/15/accepted PY - 2004/9/15/pubmed PY - 2004/12/17/medline PY - 2004/9/15/entrez SP - 351 EP - 9 JF - Pain JO - Pain VL - 111 IS - 3 N2 - Platelet-activating factor (PAF) is a potent inflammatory lipid mediator in peripheral tissues. However, its role in mediation of nociception in central nervous system is unknown. In the present study, whether PAF plays some role in pain transduction in the spinal cord was studied in mice. Intrathecal injection of PAF induced tactile pain, tactile allodynia at as low as 10 fg to 1 pg with a peak response at 100 fg, while lyso-PAF was without effect in the range of doses. Tactile allodynia induced by PAF was blocked by a PAF receptor antagonists, TCV-309, WEB 2086 and BN 50739. The expression of PAF receptor mRNA by RT-PCR was observed in DRG and spinal cord in mice. ATP P2X receptor antagonists, pyridoxalphosphate-6-azophenyl-2',4'-disulfonic acid and 2',3'-O-(2,4,6-trinitrophenyl)adenosine 5-triphosphate, NMDA receptor antagonist, MK 801 and nitric oxide synthetase inhibitor, 7-nitroindazole blocked the PAF-induced tactile allodynia. PAF-induced tactile allodynia and thermal hyperalgesia disappeared in neonatally capsaicin-treated adult mice, while tactile allodynia but not thermal hyperalgesia induced by intrathecally injected alpha,beta-methylene ATP, a P2X receptor agonist, was capsaicin-insensitive. The present study demonstrated that PAF is a potent inducer of tactile allodynia and thermal hyperalgesia at the level of the spinal cord. PAF-evoked tactile allodynia is suggested to be mediated by ATP and the following NMDA and NO cascade through capsaicin-sensitive fiber, different from exogenously injected alpha,beta-methylene ATP which is insensitive to capsaicin treatment. SN - 0304-3959 UR - https://www.unboundmedicine.com/medline/citation/15363879/Development_of_tactile_allodynia_and_thermal_hyperalgesia_by_intrathecally_administered_platelet_activating_factor_in_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0304-3959(04)00343-4 DB - PRIME DP - Unbound Medicine ER -