Enhanced wind-up of the C-fiber-mediated nociceptive flexor reflex movement following painful diabetic neuropathy in mice
Enhanced wind-up of the C-fiber-mediated nociceptive flexor reflex movement following painful diabetic neuropathy in mice
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DOI：
10.1254/jphs.fp0040785
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发表时间：
2005-02-01
影响因子：
3.5
通讯作者：
Ono, H
中科院分区：
文献类型：
--
作者：
Kimura, S;Tanabe, M;Ono, H
我们检查了在使用链脲佐菌素（STZ）治疗后发生触觉异常性疼痛的糖尿病小鼠的伤害性屈肌戒断反应的上升。在对照组和stz治疗的小鼠中，通过对脚趾腹侧的c纤维强度的电刺激同时激活Adelta-和c -纤维，引发了由同侧后爪的短潜伏期和长潜伏期运动组成的双相戒断反射，这些运动分别由Adelta-和c -纤维的激活介导。不同刺激强度引起的各反射运动的激活阈值和反射振幅在对照组和糖尿病小鼠之间无显著差异。然而，在糖尿病小鼠中，重复条件刺激（CS）引起了c纤维介导的运动和早期饱和的更大的发条。在对照组和糖尿病小鼠中，CS没有引起或偶尔引起adelta纤维介导的运动的轻微卷曲。此外，在正常小鼠的adelta纤维和c纤维介导的运动中均观察到cs后促进作用，反映了长时间的兴奋性增加，而糖尿病小鼠仅在c纤维介导的运动中观察到显著的cs后促进作用，这可能反映了棘上降作用。糖尿病小鼠脊髓神经元兴奋性的这种变化可能代表了疼痛性糖尿病神经病变的某些方面。
We examined wind-up of the nociceptive flexor withdrawal responses in diabetic mice that had developed tactile allodynia after treatment with streptozotocin (STZ). In control and STZ-treated mice, simultaneous activation of Adelta- and C-fibers by electrical stimuli at C-fiber intensity delivered to the ventral aspect of the toe elicited a biphasic withdrawal reflex composed of short- and long-latency movements of the ipsilateral hind paw that were respectively mediated by activation of Adelta- and C-fibers. There were no significant differences between control and diabetic mice in the activation threshold of each reflex movement or the amplitude of reflexes elicited by various stimulus intensities. However, a repetitive conditioning stimulus (CS) elicited significantly greater wind-up of the C-fiber-mediated movement and early saturation of wind-up in diabetic mice. In both control and diabetic mice, the CS elicited no or occasionally slight wind-up of the Adelta-fiber-mediated movement. Moreover, post-CS facilitation, which reflects the prolonged excitability increase, was observed in both Adelta-fiber- and C-fiber-mediated movements of control mice, whereas significant post-CS facilitation was only obtained in the C-fiber-mediated movement of diabetic mice, which may reflect supraspinal descending influences. Such changes in the excitability of spinal neurons in diabetic mice may represent some aspect of painful diabetic neuropathy.