Interferon-gamma and neuropathy: balance between pain and neuroprotection  

作　　者：Valentina Ferrara Alessandra Toti Carla Ghelardini Lorenzo Di Cesare Mannelli 

机构地区：[1]Department of Neuroscience,Psychology,Drug Research and Child Health-NEUROFARBA-Pharmacology and Toxicology Section,University of Florence,Florence,Italy

出　　处：《Neural Regeneration Research》2022年第12期2700-2701,共2页中国神经再生研究（英文版）

摘　　要：Chronic pain is sustained by a phenomenon of hyper-activation of nociceptive neurons both at peripheral(peripheral sensitization)and central(central sensitization)levels.The onset and maintenance of pain,however,is to be found in the interaction among the various cell populations in the nervous tissue including neurons and glia(Nam et al.,2016).The pathogenesis of neuropathic pain is extremely complex depending on the primary cause of nerve damage,e.g.traumatic nerve injury is associated with a robust inflammatory response while chemotherapy-induced pain is characterized by a modest phlogistic component(Di Cesare Mannelli et al.,2013).Despite these differences,a powerful common concept to explain the cellular mechanisms underlying pain is the activation of glia.

关 键 词：PAIN SUSTAINED 

分 类 号：R402[医药卫生—临床医学]