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Microglia: a newly discovered role in visceral hypersensitivity?

Published online by Cambridge University Press:  13 April 2007

Carl Y. Saab ,
Jing Wang ,
Chunping Gu ,
Kirsten N. Garner  and
Elie D. Al-Chaer
Carl Y. Saab
Affiliation:
Department of Surgery, Rhode Island Hospital & Brown Medical School, Providence, USA
Jing Wang
Affiliation:
Center for Pain Research, Department of Pediatrics, Neurobiology and Developmental Sciences, University of Arkansas for Medical Sciences, Little Rock, USA
Chunping Gu
Affiliation:
Center for Pain Research, Department of Pediatrics, Neurobiology and Developmental Sciences, University of Arkansas for Medical Sciences, Little Rock, USA
Kirsten N. Garner
Affiliation:
Center for Pain Research, Department of Pediatrics, Neurobiology and Developmental Sciences, University of Arkansas for Medical Sciences, Little Rock, USA
Elie D. Al-Chaer*
Affiliation:
Center for Pain Research, Department of Pediatrics, Neurobiology and Developmental Sciences, University of Arkansas for Medical Sciences, Little Rock, USA
*
Correspondence should be addressed to Elie D. Al-Chaer MS PhD JD Associate Professor, Departments of Pediatrics, Neurobiology and Developmental Sciences, University of Arkansas for Medical Sciences, 1403 West Markham, Slot 842, Little Rock, AR 72205, USA phone: +1 501 526 7828 fax: +1 501 526 7862 email: [email protected]
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Abstract

Given the growing body of evidence for a role of glia in pain modulation, it is plausible that the exaggerated visceral pain in chronic conditions might be regulated by glial activation. In this study, we have investigated a possible role for microglia in rats with chronic visceral hypersensitivity and previously documented altered neuronal function. Experiments were performed on adult male Sprague-Dawley rats pre-treated with neonatal colon irritation (CI) and on control rats. Effects of fractalkine (FKN, a chemokine involved in neuron-to-microglia signaling) and of minocycline (an inhibitor of microglia) on visceral sensitivity were examined. Visceral sensitivity was assessed by recording the electromyographic (EMG) responses to graded colorectal distension (CRD) in mildly sedated rats. Responses to CRD were recorded before and after injection of FKN, minocycline or vehicle. Somatic thermal hyperalgesia was measured by latency of paw withdrawal to radiant heat. The pattern and intensity of microglial distribution at L6–S2 in the spinal cord was also compared in rats with CI and controls by fluorescence microscopy using OX-42. Results show that: (1) FKN significantly facilitated EMG responses to noxious CRD by >52% in control rats. FKN also induced thermal hyperalgesia in control rats, consistent with previous reports; (2) minocycline significantly inhibited EMG responses to noxious CRD by >70% in rats with CI compared to controls 60 min after injection. The anti-nociceptive effect of minocycline lasted for 180 min in rats with CI, reaching peak values 60 min after injection. Our results show that FKN enhances visceral and somatic nociception, whereas minocycline inhibits visceral hypersensitivity in chronically sensitized rats, which indicates a role for microglia in visceral hypersensitivity.

Keywords

Visceral painhypersensitivityneonatal injurycolonmicroglia
Type
Research Article
Information
Neuron Glia Biology , Volume 2 , Issue 4 , November 2006 , pp. 271 - 277
Copyright
Copyright © Cambridge University Press 2007

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