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损伤性放电在大鼠神经性疼痛行为诱导中的作用。

The role of injury discharge in the induction of neuropathic pain behavior in rats.

作者信息

Seltzer Ze'ev, Beilin BenZion, Ginzburg Ruth, Paran Yoav, Shimko Thomas

机构信息

Departments of Physiology, Faculty of Dental Medicine, Hebrew University of Jerusalem, JerusalemIsrael Departments of Anesthesiology, Hasharon Hospital, Petah-TiqvaIsrael.

出版信息

Pain. 1991 Sep;46(3):327-336. doi: 10.1016/0304-3959(91)90115-E.

DOI:10.1016/0304-3959(91)90115-E
PMID:1758712
Abstract

When sensory fibers are damaged, a discharge of impulses is emitted, which can last up to a few minutes. In the present study, we examined whether this injury discharge plays a role in triggering 'autotomy'--a behavior involving self-injury in animals that is induced by total denervation of a hind paw. Sensory input from the sciatic and saphenous neuroma is thought to elicit chronic pain sensations which cause the rat to injure the hind paw. In the present experiments: (1) injury discharge was prevented by using a local anesthetic block and (2) injury discharge was artificially prolonged by delivering 150 electrical pulses to the nerve just prior to transection, at a strength sufficient to drive A- and C-fibers. In one group of animals, the nerve was stimulated at 0.5 Hz at which frequency a synchronous, repetitive activity in C-fibers augments the response of some nociceptive dorsal horn neurons by temporal summation ('wind-up'). In 2 other groups, the sciatic nerve was stimulated at 0.1 Hz and 10 Hz. The results show that blocking injury discharge significantly delayed the average time of onset of autotomy and suppressed it in magnitude compared to control rats. In contrast, electrical stimulation, especially at the 'wind-up' frequency, significantly shortened the onset of autotomy and enhanced its severity. Thus, in spite of its short duration, injury discharge affects the subsequent development of neuropathic pain related behavior.

摘要

当感觉纤维受损时,会发出一连串的冲动,这种冲动可持续长达几分钟。在本研究中,我们研究了这种损伤放电是否在引发“自残”中起作用——自残是一种动物自我伤害行为,由后爪完全去神经支配诱发。坐骨神经和隐神经瘤的感觉输入被认为会引发慢性疼痛感觉,导致大鼠伤害后爪。在本实验中:(1)通过局部麻醉阻滞来防止损伤放电,(2)在横断神经之前,以足以驱动A纤维和C纤维的强度向神经施加150个电脉冲,人为延长损伤放电。在一组动物中,以0.5赫兹的频率刺激神经,在这个频率下,C纤维中的同步重复活动通过时间总和(“wind-up”)增强一些伤害性背角神经元的反应。在另外两组中,分别以0.1赫兹和10赫兹的频率刺激坐骨神经。结果表明,与对照大鼠相比,阻断损伤放电显著延迟了自残的平均起始时间,并在程度上抑制了自残行为。相反,电刺激,尤其是在“wind-up”频率下的刺激,显著缩短了自残的起始时间并增强了其严重程度。因此,尽管损伤放电持续时间短,但它会影响随后神经性疼痛相关行为的发展。

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