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Activation of p38 mitogen-activated protein kinase in spinal microglia contributes to incision-induced mechanical allodynia.
Anesthesiology. 2009 Jan; 110(1):155-65.A

Abstract

BACKGROUND

Recent studies have implicated the activation of stress-activated mitogen-activated protein kinase (MAPK) p38 in spinal microglial cells for development of neuropathic and inflammatory pain. The aim of the present study was to investigate whether phosphorylation of p38 (p-p38) also mediates mechanical allodynia and thermal hyperalgesia induced by plantar incision.

METHODS

After rats received a plantar incision surgery, mechanical allodynia and thermal hyperalgesia were determined by von Frey filaments and radiant heat, respectively, and the number of p-p38 immunoreactive cells in the dorsal horn was quantified to determine p38 activation at different time points after incision. The p38 inhibitor FR167653 was administered intrathecally 30 min before hind paw plantar incision to determine the role of p38 in postoperative pain.

RESULTS

A significant increase in number of p-p38 immunoreactive cells was observed in the ipsilateral L4-5 spinal dorsal horn from 1 h to 3 days after the incision. p-p38 was found predominantly in microglia. However, microglial activation (assessed by OX-42 upregulation) was not evident until 3 days after plantar incision. Intrathecal pretreatment of FR167653 attenuated incision-induced mechanical allodynia from 1 h to day 2 and significantly reduced activation of p38 in the dorsal horn 1 day after plantar incision. However, FR167653 only inhibited heat hyperalgesia at an early time point.

CONCLUSIONS

Plantar incision-induced mechanical allodynia can be prevented by the p38 inhibitor. Our results suggest that p38 activation in spinal microglia play a role in incision-induced mechanical allodynia in rats. Therefore, p38 inhibition may be useful in treating postsurgical pain.

Authors+Show Affiliations

Graduate Institute of Medical Sciences, and School of Medicine, Taipei Medical University, Taipei, Taiwan.No 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)

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

Language

eng

PubMed ID

19104183

Citation

Wen, Yeong-Ray, et al. "Activation of P38 Mitogen-activated Protein Kinase in Spinal Microglia Contributes to Incision-induced Mechanical Allodynia." Anesthesiology, vol. 110, no. 1, 2009, pp. 155-65.
Wen YR, Suter MR, Ji RR, et al. Activation of p38 mitogen-activated protein kinase in spinal microglia contributes to incision-induced mechanical allodynia. Anesthesiology. 2009;110(1):155-65.
Wen, Y. R., Suter, M. R., Ji, R. R., Yeh, G. C., Wu, Y. S., Wang, K. C., Kohno, T., Sun, W. Z., & Wang, C. C. (2009). Activation of p38 mitogen-activated protein kinase in spinal microglia contributes to incision-induced mechanical allodynia. Anesthesiology, 110(1), 155-65. https://doi.org/10.1097/ALN.0b013e318190bc16
Wen YR, et al. Activation of P38 Mitogen-activated Protein Kinase in Spinal Microglia Contributes to Incision-induced Mechanical Allodynia. Anesthesiology. 2009;110(1):155-65. PubMed PMID: 19104183.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Activation of p38 mitogen-activated protein kinase in spinal microglia contributes to incision-induced mechanical allodynia. AU - Wen,Yeong-Ray, AU - Suter,Marc R, AU - Ji,Ru-Rong, AU - Yeh,Geng-Chang, AU - Wu,Yen-Sheng, AU - Wang,Kuo-Ching, AU - Kohno,Tatsuro, AU - Sun,Wei-Zen, AU - Wang,Chia-Chuan, PY - 2008/12/24/entrez PY - 2008/12/24/pubmed PY - 2009/1/23/medline SP - 155 EP - 65 JF - Anesthesiology JO - Anesthesiology VL - 110 IS - 1 N2 - BACKGROUND: Recent studies have implicated the activation of stress-activated mitogen-activated protein kinase (MAPK) p38 in spinal microglial cells for development of neuropathic and inflammatory pain. The aim of the present study was to investigate whether phosphorylation of p38 (p-p38) also mediates mechanical allodynia and thermal hyperalgesia induced by plantar incision. METHODS: After rats received a plantar incision surgery, mechanical allodynia and thermal hyperalgesia were determined by von Frey filaments and radiant heat, respectively, and the number of p-p38 immunoreactive cells in the dorsal horn was quantified to determine p38 activation at different time points after incision. The p38 inhibitor FR167653 was administered intrathecally 30 min before hind paw plantar incision to determine the role of p38 in postoperative pain. RESULTS: A significant increase in number of p-p38 immunoreactive cells was observed in the ipsilateral L4-5 spinal dorsal horn from 1 h to 3 days after the incision. p-p38 was found predominantly in microglia. However, microglial activation (assessed by OX-42 upregulation) was not evident until 3 days after plantar incision. Intrathecal pretreatment of FR167653 attenuated incision-induced mechanical allodynia from 1 h to day 2 and significantly reduced activation of p38 in the dorsal horn 1 day after plantar incision. However, FR167653 only inhibited heat hyperalgesia at an early time point. CONCLUSIONS: Plantar incision-induced mechanical allodynia can be prevented by the p38 inhibitor. Our results suggest that p38 activation in spinal microglia play a role in incision-induced mechanical allodynia in rats. Therefore, p38 inhibition may be useful in treating postsurgical pain. SN - 1528-1175 UR - https://www.unboundmedicine.com/medline/citation/19104183/Activation_of_p38_mitogen_activated_protein_kinase_in_spinal_microglia_contributes_to_incision_induced_mechanical_allodynia_ L2 - http://anesthesiology.pubs.asahq.org/article.aspx?doi=10.1097/ALN.0b013e318190bc16 DB - PRIME DP - Unbound Medicine ER -