Minocycline treatment inhibits microglial activation and alters spinal levels of endocannabinoids in a rat model of neuropathic pain

doi:10.1186/1744-8069-5-35

Molecular Pain

Volume 5

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Guasti L
Richardson D
Jhaveri M
Eldeeb K
Barrett D
Elphick MR
Alexander SP
Kendall D
Michael GJ
Chapman V

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Richardson D
Jhaveri M
Eldeeb K
Barrett D
Elphick MR
Alexander SP
Kendall D
Michael GJ
Chapman V
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Minocycline treatment inhibits microglial activation and alters spinal levels of endocannabinoids in a rat model of neuropathic pain

Leonardo Guasti¹^,2^* , Denise Richardson³^,5^* , Maulik Jhaveri³ , Khalil Eldeeb³ , David Barrett⁴ , Maurice R Elphick¹ , Stephen PH Alexander³ , David Kendall³ , Gregory J Michael² and Victoria Chapman³

¹School of Biological and Chemical Sciences, Queen Mary University of London, UK

²Neuroscience Centre, Institute of Cell and Molecular Science, Queen Mary University of London, UK

³School of Biomedical Sciences, University of Nottingham, UK

⁴School of Pharmacy, University of Nottingham, UK

⁵Pfizer, Ramsgate Road, Sandwich, Kent, UK

author email corresponding author email* Contributed equally

Molecular Pain 2009, 5:35doi:10.1186/1744-8069-5-35


Published:	1 July 2009

Abstract

Activation of spinal microglia contributes to aberrant pain responses associated with neuropathic pain states. Endocannabinoids (ECs) are present in the spinal cord, and inhibit nociceptive processing; levels of ECs may be altered by microglia which modulate the turnover of endocannabinoids in vitro. Here, we investigate the effect of minocycline, an inhibitor of activated microglia, on levels of the endocannabinoids anandamide and 2-arachidonoylglycerol (2-AG), and the related compound N-palmitoylethanolamine (PEA), in neuropathic spinal cord. Selective spinal nerve ligation (SNL) in rats resulted in mechanical allodynia and the presence of activated microglia in the ipsilateral spinal cord. Chronic daily treatment with minocycline (30 mg/kg, ip for 14 days) significantly reduced the development of mechanical allodynia at days 5, 10 and 14 post-SNL surgery, compared to vehicle-treated SNL rats (P < 0.001). Minocycline treatment also significantly attenuated OX-42 immunoreactivity, a marker of activated microglia, in the ipsilateral (P < 0.001) and contralateral (P < 0.01) spinal cord of SNL rats, compared to vehicle controls. Minocycline treatment significantly (P < 0.01) decreased levels of 2-AG and significantly (P < 0.01) increased levels of PEA in the ipsilateral spinal cord of SNL rats, compared to the contralateral spinal cord. Thus, activation of microglia affects spinal levels of endocannabinoids and related compounds in neuropathic pain states.