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Activation of astrocytes in the spinal cord contributes to the development of bilateral allodynia after peripheral nerve injury in rats.
Brain Res. 2010 Dec 02; 1363:72-80.BR

Abstract

Activation of spinal cord microglia and astrocytes after peripheral nerve injury contributes to the development of behavioral hypersensitivity. Suppression of spinal cord glial activation attenuates the development of nerve injury-induced allodynia. The contribution of spinal cord glia to existing allodynia, however, is not known. We investigated whether intrathecally administered propentofylline, a glial inhibitor, reverses existing allodynia after nerve injury. Male Sprague-Dawley rats underwent L5 spinal nerve transection, and mechanical allodynia was assessed by measuring hind paw withdrawal thresholds bilaterally using von Frey filaments. Rats received either saline or propentofylline (1, 3, and 10 μg/d) for 7 days (days 0-7) by intrathecal infusion with an osmotic minipump. Other groups of rats received either intrathecal infusion of saline or propentofylline (10 μg/d) for 7 days on days 14-21 or 60-67 after surgery. After completing the intrathecal infusion, lumbar spinal cord sections were assessed for immunostaining of astrocytic glial fibrillary acidic protein and microglial OX-42. Propentofylline infusion on days 0-7 suppressed development of allodynia in both the ipsilateral and contralateral hind paws in a dose-dependent manner. Propentofylline treatment on days 14-21 or 60-67 did not reverse existing allodynia. Propentofylline infusion (10 μg/d) inhibited astrocytic activation bilaterally on days 0-7, 14-21, and 60-67 and inhibited microglial activation on days 14-21 but not on days 0-7 and 60-67. These results suggest that activation of spinal glia, especially astrocytes, dominantly contributes to the development of neuropathic pain and also to mirror-image pain.

Authors+Show Affiliations

Department of Anesthesiology, Gunma University Graduate School of Medicine, 3-39-22, Showa-machi, Maebashi, Gunma 371-8511, Japan. hobata@showa.gunma-u.ac.jpNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

20932955

Citation

Obata, Hideaki, et al. "Activation of Astrocytes in the Spinal Cord Contributes to the Development of Bilateral Allodynia After Peripheral Nerve Injury in Rats." Brain Research, vol. 1363, 2010, pp. 72-80.
Obata H, Sakurazawa S, Kimura M, et al. Activation of astrocytes in the spinal cord contributes to the development of bilateral allodynia after peripheral nerve injury in rats. Brain Res. 2010;1363:72-80.
Obata, H., Sakurazawa, S., Kimura, M., & Saito, S. (2010). Activation of astrocytes in the spinal cord contributes to the development of bilateral allodynia after peripheral nerve injury in rats. Brain Research, 1363, 72-80. https://doi.org/10.1016/j.brainres.2010.09.105
Obata H, et al. Activation of Astrocytes in the Spinal Cord Contributes to the Development of Bilateral Allodynia After Peripheral Nerve Injury in Rats. Brain Res. 2010 Dec 2;1363:72-80. PubMed PMID: 20932955.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Activation of astrocytes in the spinal cord contributes to the development of bilateral allodynia after peripheral nerve injury in rats. AU - Obata,Hideaki, AU - Sakurazawa,Shinobu, AU - Kimura,Masafumi, AU - Saito,Shigeru, Y1 - 2010/10/25/ PY - 2010/04/06/received PY - 2010/08/23/revised PY - 2010/09/29/accepted PY - 2010/10/12/entrez PY - 2010/10/12/pubmed PY - 2011/2/25/medline SP - 72 EP - 80 JF - Brain research JO - Brain Res VL - 1363 N2 - Activation of spinal cord microglia and astrocytes after peripheral nerve injury contributes to the development of behavioral hypersensitivity. Suppression of spinal cord glial activation attenuates the development of nerve injury-induced allodynia. The contribution of spinal cord glia to existing allodynia, however, is not known. We investigated whether intrathecally administered propentofylline, a glial inhibitor, reverses existing allodynia after nerve injury. Male Sprague-Dawley rats underwent L5 spinal nerve transection, and mechanical allodynia was assessed by measuring hind paw withdrawal thresholds bilaterally using von Frey filaments. Rats received either saline or propentofylline (1, 3, and 10 μg/d) for 7 days (days 0-7) by intrathecal infusion with an osmotic minipump. Other groups of rats received either intrathecal infusion of saline or propentofylline (10 μg/d) for 7 days on days 14-21 or 60-67 after surgery. After completing the intrathecal infusion, lumbar spinal cord sections were assessed for immunostaining of astrocytic glial fibrillary acidic protein and microglial OX-42. Propentofylline infusion on days 0-7 suppressed development of allodynia in both the ipsilateral and contralateral hind paws in a dose-dependent manner. Propentofylline treatment on days 14-21 or 60-67 did not reverse existing allodynia. Propentofylline infusion (10 μg/d) inhibited astrocytic activation bilaterally on days 0-7, 14-21, and 60-67 and inhibited microglial activation on days 14-21 but not on days 0-7 and 60-67. These results suggest that activation of spinal glia, especially astrocytes, dominantly contributes to the development of neuropathic pain and also to mirror-image pain. SN - 1872-6240 UR - https://www.unboundmedicine.com/medline/citation/20932955/Activation_of_astrocytes_in_the_spinal_cord_contributes_to_the_development_of_bilateral_allodynia_after_peripheral_nerve_injury_in_rats_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-8993(10)02171-2 DB - PRIME DP - Unbound Medicine ER -