Growing evidence suggests that astroglia, a major non-neuronal cell type in the brain, contribute to the development of persistent pain. We have studied nerve injury-induced astrocytic responses in the rostral ventromedial medulla (RVM), a pivotal brain stem structure involved in descending pain modulation. Following peripheral nerve injury, astrocytic activity is altered, as indicated by increased expression of astroglial markers and down regulation of the astrocytic glutamate transporter GLT-1. These changes correlated with neuropathic pain behaviors. IL-1beta and chemokine monocyte chemoattractant protein-1 (MCP-1, CCL2) are likely mediators of neuron-glial interactions. Our findings suggest that reciprocal interactions between neurons and astroglia play a critical role in descending facilitation of neuropathic pain.
展开▼
