【摘 要】
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Acute pain plays an important physiological role as a warning system for the body.However,in many patients,nerve damage leads to neuropathic pain that can last for years and disrupts their quality of life.Unfortunately,neuropathic pain mechanisms remain l
【机 构】
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Department of Molecular,Cellular,and Developmental Biology,University of Michigan,Ann Arbor,MI 48109
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Acute pain plays an important physiological role as a warning system for the body.However,in many patients,nerve damage leads to neuropathic pain that can last for years and disrupts their quality of life.Unfortunately,neuropathic pain mechanisms remain largely unknown and this condition is largely resistant to available treatments.Developing new strategies to treat neuropathic pain depends on a better understanding of the molecular,cellular,and circuit mechanisms underlying the transition from the acute to the chronic pain state,which involves changes not only within the spinal cord and the brain,but also the initiation site of pain—primary sensory neurons.Emerging experimental evidence has shown perturbed transcriptional profiles following peripheral neuropathy that might contribute to the pathophysiology of neuropathic pain[1-3].Alhough these studies provide insights into axotomy-induced transcriptome remodeling,they have a limited ability to define the diverse and heterogeneous subclasses of sensory neurons that respond with perturbed transcriptomes to nerve damage and contribute to the pathophysiology of neuropathic pain.
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