Spinal Cord Neural Plasticity in Chronic Pain and its Clinical Implication
Authors: Jacqueline R. Dauch and Hsinlin T. Cheng
Abstract: Chronic pain is a common medical condition that causes significant physical and psychological disabilities to the general population. Although there is a high prevalence of chronic pain, effective treatments are still in urgent need to treat the condition. Fortunately, researchers have shed light on the molecular mechanism of painful chronic conditions for both inflammatory and neuropathic pain through recent animal studies. Through these studies, researchers have discovered that the spinal cord is an important relay center to integrate peripheral painful inputs and propagate signals to the brain. In painful conditions, peripheral nociceptors transmit afferent painful signals to the spinal cord dorsal horn (SCDH) by releasing neurotransmitters from presynaptic terminals. These neurotransmitters cross the synapse and activate the corresponding receptors on the postsynaptic terminals of neurons and glial cells in the SCDH. These events induce multiple inflammatory and neuropathic processes in the SCDH, as well as trigger modification and plasticity of local neural circuits. In addition, the activation of glial cells, including astrocytes and microglia in SCDH, contribute to the persistence of increased nociception through the enhancement of local actions of cytokines and chemokines. As a result of such molecular modifications, painful signals are often amplified and prolonged, a phenomenon known as central sensitization. In this review, the molecular events associated with central sensitization and their clinical implications are discussed.