Chemical stimulation of the intracranial dura induces enhanced responses to facial stimulation in brain stem trigeminal neurons
Chemical stimulation of the intracranial dura induces enhanced responses to facial stimulation in brain stem trigeminal neurons
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DOI：
10.1152/jn.1998.79.2.964
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发表时间：
1998-02-01
影响因子：
2.5
通讯作者：
Strassman, AM
中科院分区：
文献类型：
--
作者：
Burstein, R;Yamamura, H;Strassman, AM
支配颅内脑膜的三叉神经初级传入神经元的化学激活和敏化被认为是某些头痛的可能原因。然而，这种致敏作用不能解释经常伴随头痛的颅外超敏反应。本研究的目的是检验脑膜感觉神经元的化学激活和敏化可以导致从硬脑膜和皮肤接收会聚输入的中央三叉神经元的激活和敏化的假设。通过记录尾侧核中23个[16个宽动态范围（WDR），5个高阈值（HT）和2个低阈值（LT）]硬膜敏感神经元对硬脑膜感受野的机械刺激和局部应用炎性介质或酸性试剂后对皮肤感受野的机械和热刺激的反应性变化，研究了这一假设。在70%的神经元中记录到对短暂化学刺激的反应，大多数是短暂的，仅持续刺激的持续时间。化学刺激硬膜20分钟后，出现以下变化：（1）95%的神经元对硬膜机械压入的敏感性显著增加;硬脑膜压陷阈值在1.57 ~ 0.49g之间（平均值，P < 0.0001），并且对相同刺激的反应幅度增加2 - 4倍，2）80%的神经元表现出皮肤机械敏感性的显著增加：他们对刷牙和压力的反应增加了2.5-（P < 0.05）和1.6倍（3）75%的神经元表现出皮肤温度敏感性的显著增加：他们皮肤缓慢发热的阈值从43.7 ± 0.7 ℃变为40.3 ± 0.7 ℃，（P < 0.005）和从23.7 +/- 3.3至29.2 +/- 1.8 ℃缓慢冷却（4）硬膜感受野在30 min内扩大，皮肤感受野在2-4 h内扩大;（5）在WDR和HT神经元中有持续活动，而在LT神经元中无。将利多卡因应用于硬脑膜可消除对硬脑膜刺激的反应，但对皮肤刺激的反应增加影响甚微（提示中枢机制参与维持致敏状态）。逆向激活（电流
Chemical activation and sensitization of trigeminal primary afferent neurons innervating the intracranial meninges have been postulated as possible causes of certain headaches. This sensitization, however, cannot explain the extracranial hypersensitivity that often accompanies headache. The goal of this study was to test the hypothesis that chemical activation and sensitization of meningeal sensory neurons can lead to activation and sensitization of central trigeminal neurons that receive convergent input from the dura and skin. This hypothesis was investigated by recording changes in the responsiveness of 23 [16 wide-dynamic range (WDR), 5 high threshold (HT), and 2 low threshold (LT)] dura-sensitive neurons in nucleus caudalis to mechanical stimulation of their dural receptive fields and to mechanical and thermal stimulation of their cutaneous receptive fields after local application of inflammatory mediators or acidic agents to the dura. Responses to brief chemical stimulation were recorded in 70% of the neurons most were short, lasting the duration of the stimulus only. Twenty minutes after chemical stimulation of the dura, the following changes occurred: 1) 95% of the neurons showed significant increases in sensitivity to mechanical indentation of the dura: their thresholds to dural indentation changed from 1.57 to 0.49 g (means, P < 0.0001), and the response magnitude to identical stimuli increased by two-to four fold, 2) 80% of the neurons showed significant increases in cutaneons mechanosensitivity: their responses to brush and pressure increased 2.5- (P < 0.05) and 1.6-fold (P < 0.05), respectively; 3) 75% of the neurons showed a significant increase in cutaneous thermosensitivity: their thresholds to slow heating of the skin changed from 43.7 +/- 0.7 to 40.3 +/- 0.7 degrees C (P < 0.005) and to slow cooling from 23.7 +/- 3.3 to 29.2 +/- 1.8 degrees C (P < 0.05); 4) dural receptive fields expanded within 30 min and cutaneous receptive fields within 2-4 h; and 5) ongoing activity developed in WDR and HT but not in LT neurons. Application of lidocaine to the dura abolished the response to dural stimulation but had minimal effect on the Increased responses to cutaneous stimulation (suggesting involvement of a central mechanism in maintaining the sensitized stale). Antidromic activation (current of