Molecular Pain
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 ResearchSelective activation of microglia in spinal cord but not higher cortical regions following nerve injury in adult mouseFuxing Zhang , Kujumon I Vadakkan , Susan S Kim , Long-Jun Wu , Yuze Shang and Min Zhuo  Department of Physiology, Faculty of Medicine, University of Toronto, University of Toronto Centre for Study of Pain, 1 King's College Circle, Toronto, Ontario M5S 1A8, Canada author email corresponding author email
Molecular Pain 2008,
4:15doi:10.1186/1744-8069-4-15 Abstract
Neuronal plasticity along the pathway for sensory transmission including the spinal cord and cortex plays an important role in chronic pain, including inflammatory and neuropathic pain. While recent studies indicate that microglia in the spinal cord are involved in neuropathic pain, a systematic study has not been performed in other regions of the central nervous system (CNS). In the present study, we used heterozygous Cx3cr1GFP/+mice to characterize the morphological phenotypes of microglia following common peroneal nerve (CPN) ligation. We found that microglia showed a uniform distribution throughout the CNS, and peripheral nerve injury selectively activated microglia in the spinal cord dorsal horn and related ventral horn. In contrast, microglia was not activated in supraspinal regions of the CNS, including the anterior cingulate cortex (ACC), prefrontal cortex (PFC), primary and secondary somatosensory cortex (S1 and S2), insular cortex (IC), amygdala, hippocampus, periaqueductal gray (PAG) and rostral ventromedial medulla (RVM). Our results provide strong evidence that nerve injury primarily activates microglia in the spinal cord of adult mice, and pain-related cortical plasticity is likely mediated by neurons. |