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. 2007 Dec 12;3:38. doi: 10.1186/1744-8069-3-38

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Copyright © 2007 Bhangoo et al; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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CCR2 receptor antagonist (CCR2 RA-[R]) administration reversed existing nociceptive behavior. Animals were subjected to a nerve demyelination injury on day 0 and nociceptive behavior was assessed for 28 days. On days 14 and 28 post-surgery, animals received 5 mg/kg CCR2 RA-[R] or 5 mg/kg of its inactive enantiomer, (CCR2 RA-[S], or saline by intraperitoneal injection, and behavioral responses were tested 1 h later. Administration of the CCR2 RA-[R] to focal nerve demyelination injured rats resulted in a significant bilateral increase of mN force required to elicit a paw withdrawal compared with vehicle-treated controls and animals subjected to CCR2 RA-[S]. Nociceptive behavior in vehicle-treated controls and animals subjected to CCR2 RA-[S] differed significantly from day 0 pre-injury baseline responses (*p < 0.01). Data represent means ± SE.