Neuronal and microglial mechanisms of neuropathic pain
1 Center for Neuron and Disease, Frontier Institute of Science and Technology, Xi'an Jiaotong University, Xi'an, China
2 Department of Physiology, Faculty of Medicine, University of Toronto Centre for the Study of Pain, University of Toronto, 1 King's College Circle, Toronto, Ontario M5S 1A8, Canada
3 Research Division, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA
4 Department of Neurobiology, Harvard Medical School and Department of Cardiology, Children's Hospital Boston, MA 02115, USA
Molecular Brain 2011, 4:31 doi:10.1186/1756-6606-4-31Published: 30 July 2011
Neuropathic pain is generally defined as a chronic pain state resulting from peripheral and/or central nerve injury. Effective treatment for neuropathic pain is still lacking, due in part to poor understanding of pathological mechanisms at the molecular level. Neuronal mechanisms of neuropathic pain, especially synaptic plasticity, are the major focus of many investigators. N-methyl-D-aspartate (NMDA) receptor dependent synaptic plasticity at the spinal and cortical levels is believed to contribute to enhanced sensory responses after injury. Glial cells, including astrocytes and microglia, have recently been implicated in neuropathic pain. These glial cells form close interactions with neurons and thus may modulate nociceptive transmission under pathological conditions. In this review, we present recent progress in the study of neuronal and microglial mechanisms underlying neuropathic pain. We propose that activity-dependent neuronal plasticity is a key target for treatment in neuropathic pain.