NMDA receptor mechanisms contribute to neuroplasticity induced in caudalis nociceptive neurons by tooth pulp stimulation
NMDA receptor mechanisms contribute to neuroplasticity induced in caudalis nociceptive neurons by tooth pulp stimulation
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DOI：
10.1152/jn.1998.80.5.2621
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发表时间：
1998-11-01
影响因子：
2.5
通讯作者：
Sessle, BJ
中科院分区：
文献类型：
--
作者：
Chiang, CY;Park, SJ;Sessle, BJ
我们最近证明，将芥菜油（MO），一种小纤维兴奋剂和炎症刺激物，应用于大鼠上颌磨牙牙髓，可诱导颌骨肌电图（EMG）活动显著且持续增加，这表明中枢神经可塑性。由于小纤维传入神经，包括髓质传入神经，进入三叉神经尾侧亚核的伤害性神经元，本研究探讨了髓质应用MO是否会引起尾侧伤害性神经元的神经可塑性变化（宽动态范围和伤害特异性），以及中枢n -甲基- d -天冬氨酸（NMDA）受体机制是否参与了这些MO诱导的神经可塑性变化。在髓质表面进行10 μ 1 i.t生理盐水预处理后，将MO牙髓应用于上颌磨牙吞下后，神经元自发活动显著增加，捏和/或触觉机械感受野（RF）显著扩大，机械阈值显著降低，神经元对梯度捏刺激的反应显著增加。与药物处理大鼠相比，另一组大鼠预处理NMDA受体拮抗剂MK-801 (10 μ g/10 μ 1)，然后将MO应用于牙髓，显著减少或消除了这些MO诱导的伤害性神经元的神经可塑性变化。在另一组用生理盐水（鞘内）预处理的大鼠中，矿物油涂抹在牙髓上，在40分钟的观察期内，自发活动或射频特性没有出现任何显著变化。在其他大鼠的牙髓应用MO（经盐水预处理，鞘内）未产生尾侧低阈机械感受神经元的任何显着神经可塑性改变。这些结果表明，mo诱导的磨牙髓传入神经的激活可以在尾侧伤害神经元中产生深刻的NMDA受体相关的神经可塑性改变。这种神经可塑性改变可能导致痛觉过敏和疼痛的扩散，这可能与牙髓炎有关。
We recently demonstrated that application of mustard oil (MO), a small-fiber excitant and inflammatory irritant, to the rat maxillary molar tooth pulp induces significant and prolonged increases in jaw muscle electromyographic (EMG) activity that are suggestive of central neuroplasticity. Because small-fiber afferents, including pulp afferents, access nociceptive neurons in trigeminal (V) subnucleus caudalis, this study examined whether pulpal application of MO induces neuroplastic changes in caudalis nociceptive neurons (wide dynamic range and nociceptive specific) and whether central N-methyl-D-aspartate (NMDA) receptor mechanisms are involved in these MO-induced neuroplastic changes. After pretreatment with vehicle (saline, 10 mu 1 i.t.) to the surface of the medulla, the pulpal application of MO to the maxillary molar tooth gulp produced a significant increase in neuronal spontaneous activity, a significant expansion of the pinch and/or tactile mechanoreceptive field (RF), a significant decrease in mechanical threshold, and significant increases in neuronal responses to graded pinch stimuli. Compared with vehicle-treated rats, pretreatment with the NMDA receptor antagonist MK-801 (10 mu g/10 mu 1 i.t.) followed by MO application to the pulp in another group of rats significantly reduced or abolished these MO-induced neuroplastic changes in nociceptive neurons. In another group of rats pretreated with saline (intrathecally), mineral oil application to the pulp did not show any significant changes in spontaneous activity or RF properties over the 40-min observation period. The pulpal application of MO in other rats (pretreated with saline, intrathecally) did not produce any significant neuroplastic changes in caudalis low-threshold mechanoreceptive neurons. These results indicate that the MO-induced activation of molar pulpal afferents can produce profound NMDA receptor-related neuroplastic changes in caudalis nociceptive neurons. Such neuroplastic changes may contribute to the hyperalgesia and spread of pain that can be associated with pulpal inflammation.