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周围神经损伤后神经元变化及肾上腺素受体α1的表达

周围神经损伤后神经元变化及肾上腺素受体α1的表达

西澳大利亚莫道克大学慢性疼痛及炎性疾病研究中心Peter D. Drummond教授研究发现,神经病理性疼痛的主要原因是由早期免疫细胞浸润到损伤组织中释放的炎症介质引起。这些介质可直接或通过神经营养因子的诱导,触发围绕损伤部位神经元和其他细胞增加肾上腺素受体α1的表达。反之,被激活的肾上腺素受体α1又触发成纤维细胞和角质化细胞进一步释放生长因子和炎性介质。因此,肾上腺素受体α1的表达是这些受损细胞和再生的神经元产生炎症和疼痛的重要原因。作者认为,肾上腺素受体α1将成为损伤的周围神经出现神经性疼痛治疗的重要靶点。此观点发表在《中国神经再生研究(英文版)》2014年7月第14期杂志上。

Article: “Neuronal changes resulting in up-regulation of alpha-1 adrenoceptors after peripheral nerve injury”by Peter D. Drummond (Centre for Research on Chronic Pain and Inflammatory Diseases, Murdoch University, Perth, Western Australia, Australia).

Drummond PD. Neuronal changes resulting in up-regulation of alpha-1 adrenoceptors after peripheral nerve injury. Neural Regen Res. 2014;9(14):1337-1340.

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Neural Regen Res

Up-regulation of neuronal alpha-1 adrenoceptors after peripheral nerve injury

SUMMARY

After nerve and tissue injury, inflammatory mediators could either directly, or through the induction of neurotrophic factors, trigger increased α1-adrenoceptor expression on neurons and other cells around the site of injury. In turn, activation of α1-adrenoceptors on fibroblasts and keratinocytes may trigger further release of growth factors and inflammatory mediators. Thus, an upward spiral of α1-adrenoceptor expression on these cells and on regenerating neurons could engender an adrenergic component of inflammation and pain.

NEWS RELEASE

In a Perspectives paper published in Neural Regeneration Research (Vol. 9, No. 14), Professor Peter Drummond speculates about neuronal changes that might contribute to chronic pain after peripheral nerve injury. Professor Drummond and co-workers at Murdoch University, Perth Western Australia, discovered recently that the expression of α1-adrenoceptors increases on pain-signalling nerve fibers that survive peripheral injury. As these receptors boost neural excitability, an increase in their expression could intensify pain. After tissue injury, resident cells and other cells that migrate to the site of injury release a cocktail of inflammatory mediators and growth factors that help to prevent infection and instigate tissue repair. However, these mediators may also trigger the up-regulation of α1-adrenoceptors on resident cells and nerve fibers that survive the injury. As certain resident and migratory cells are a major source of inflammatory mediators and growth factors, the

up-regulation of α1-adrenoceptors may promote a cycle of chronic inflammation and pain. If so, blocking the 1-adrenoceptor might prove to be a useful therapeutic strategy for patients with an adrenergic component of pain after peripheral nerve injury.

Article: “Neuronal changes resulting in up-regulation of alpha-1 adrenoceptors after peripheral nerve injury”by Peter D. Drummond (Centre for Research on Chronic Pain and Inflammatory Diseases, Murdoch University, Perth, Western Australia, Australia).

Drummond PD. Neuronal changes resulting in up-regulation of alpha-1 adrenoceptors after peripheral nerve injury. Neural Regen Res. 2014;9(14):1337-1340.