Role of primary afferent nerves in allodynia caused by diabetic neuropathy in rats

Role of primary afferent nerves in allodynia caused by diabetic neuropathy in rats
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DOI:
10.1016/s0306-4522(02)00372-x
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发表时间:
2002-01-01
期刊:
影响因子:
3.3
通讯作者:
Pan, HL
Pan, HL
中科院分区:
医学3区
文献类型:
--
作者:
Khan, GM;Chen, SR;Pan, HL

文献摘要

被引文献

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有myclinated和无myclinated的传入神经都参与了糖尿病神经性疼痛的传递。虽然一般认为非肌性传入在糖尿病神经性疼痛中起重要作用,但糖尿病神经病变的病理变化主要发生在肌性A纤维中。在本研究中,我们首先研究了辣椒素敏感的C纤维在糖尿病神经病变引起的异常性疼痛的发展中的作用。然后,我们研究了糖尿病神经病理性疼痛相关的传入神经的功能变化。腹腔注射链脲佐菌素诱导大鼠糖尿病。为了消耗辣椒素敏感的C-纤维,用腹膜内树脂毒素(300 μ g/kg)处理大鼠。机械和热敏性进行了测量,使用冯弗雷长丝和辐射热刺激。从胫神经记录传入神经的单个单位活动。糖尿病大鼠出现触觉异常性疼痛,但不出现热痛觉过敏。树脂毒素治疗并没有显着改变异常性疼痛的程度和时程。用树脂毒素后处理也未能减轻糖尿病大鼠的异常性疼痛。电生理记录显示异位放电和较高的自发活动,主要是在A δ和A β纤维传入在糖尿病大鼠,无论树脂毒素治疗。此外,这些传入纤维具有较低的激活阈值和对机械刺激的增强反应。因此,我们的研究表明,辣椒素敏感的C-纤维传入在糖尿病大鼠模型的异常性疼痛的发展中是不需要的。我们的电生理数据提供了大量的新证据表明,异常的感觉输入从A δ和A β纤维传入可能在糖尿病神经病理性疼痛中发挥重要作用。(C)2002年IBRO。由Elsevier Science Ltd.出版,版权所有。
Both myclinated and unmyclinated afferents are implicated in transmitting diabetic neuropathic pain. Although unmyclinated afferents are generally considered to play a significant role in diabetic neuropathic pain, pathological changes in diabetic neuropathy occur mostly in myclinated A-fibers. In the present study, we first examined the role of capsaicin-sensitive C-fibers in the development of allodynia induced by diabetic neuropathy. We then studied the functional changes of afferent nerves pertinent to diabetic neuropathic pain. Diabetes was induced in rats by i.p. streptozotocin. To deplete capsaicin-sensitive C-fibers, rats were treated with i.p. resiniferatoxin (300 mug/kg). Mechanical and thermal sensitivities were measured using von Frey filaments and a radiant heat stimulus. Sing-le-unit activity of afferents was recorded from the tibial nerve. Tactile allodynia, but not thermal hyperalgesia, developed in diabetic rats. Resiniferatoxin treatment did not alter significantly the degree and time course of allodynia. Post-treatment with resiniferatoxin also failed to attenuate allodynia in diabetic rats. The electrophysiological recordings revealed ectopic discharges and a higher spontaneous activity mainly in Adelta- and Abeta-fiber afferents in diabetic rats regardless of resiniferatoxin treatment. Furthermore, these afferent fibers had a lower threshold for activation and augmented responses to mechanical stimuli. Thus, our study suggests that capsaicin-sensitive C-fiber afferents are not required in the development of allodynia in this rat model of diabetes. Our electrophysiological data provide substantial new evidence that the abnormal sensory input from Adelta- and Abeta-fiber afferents may play an important role in diabetic neuropathic pain. (C) 2002 IBRO. Published by Elsevier Science Ltd. All rights reserved.