Peripherial tissue and nerve injury leads to chronic pain symptoms, including spontaneous pain, allodynia and hyperalgesia. More than a century it has been realized that peripheral and central neural mechanisms interact extensively to reinforce these pathological changes that contributed to chronic pain. Particular important in many neuropathic pains is the involvement of sympathetic nervous system, either through development of abnormal sympathetic function or through its effects on abnormally functioning afferent nerves. Under normal conditions some catecholaminergic fibers innervate primary afferent neurons and there is no significant functional communication between sympathetic fibers and sensory neurons. However, sensory neurons and nociceptors may develop abnormal responsiveness to sympathetic agonists and the activation of postganglionic sympathetic efferent axons in certain neuropathic pain state after tissue inflammation and nerve lesion.With a model of chronically compressed dorsal root ganglion(CCD), the present study was undertaken to examine the adrenosensitivity of chronically compressed DRG neurons, discuss the contribution of PKA and other active substances in adrenosensitation as well, and provide bases for further investigating cellular mechanisms of sympathetic-dependent pain.Main results...
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