TIME COURSE OF MECHANOSENSITIVITY CHANGES IN ARTICULAR AFFERENTS DURING A DEVELOPING EXPERIMENTAL ARTHRITIS
TIME COURSE OF MECHANOSENSITIVITY CHANGES IN ARTICULAR AFFERENTS DURING A DEVELOPING EXPERIMENTAL ARTHRITIS
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DOI：
10.1152/jn.1988.60.6.2180
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发表时间：
1988-12-01
影响因子：
2.5
通讯作者：
SCHMIDT, RF
中科院分区：
文献类型：
--
作者：
SCHAIBLE, HG;SCHMIDT, RF
在37只猫中，从右膝关节的内侧关节神经（MAN）的单传入单位进行氯醛糖记录。首先，当关节处于正常状态时，这些单元的机械敏感性被表征。此后，在连续观察下保持传入，通过将高岭土和角叉菜胶注射到关节腔内来诱导实验性关节炎。发展中的关节炎的影响，包括时间过程的变化进行了研究，对低和高阈值单位和传入，在正常关节中没有mechanosensitivity。关节炎增加了大多数低阈值单位的机械敏感性，即，在正常关节已经对工作范围内的运动做出反应的单位中。16个厚髓鞘II组中有12个，10个细髓鞘III组中有10个，3个无髓鞘IV组传入神经中有1个对运动的反应增强。在大多数情况下，在注射炎性化合物后的第一个小时内发生反应增强，有时在注射后立即开始。在随后的2-4小时内观察到机械敏感性的进一步上升。在大多数第三组单位增强反应的运动伴随着诱导或增加静息放电。在1组II和1组IV单位自发活动的情况下，没有任何变化的运动敏感性。炎症导致高阈值传入的机械敏感性增强，即，在正常关节仅对超出膝盖工作范围的有害运动做出反应的单位中。一组II，10组12 III，5组10 IV单位的这种类型的成为响应于在关节炎的发展过程中，在大多数情况下，在第二至第三个小时内诱导炎症后的进一步增加工作范围内的运动，在这些单位的高比例休息活动也被诱导。少数高阈值单位自发放电，但没有反应的工作范围内的运动。静息活动发展的时间过程与机械阈值降低的时间过程相似。实验性关节炎在2个III组单位中的1个和14个IV组单位中的10个中诱导传入活动，这些单位在正常关节中对局部机械刺激和无害/有害运动无反应（但对靠近关节动脉内施加的KCl溶液团有反应）。一些纤维开始对工作范围内的运动做出反应，并发展出休息活动，一些纤维开始只对发炎膝盖的极端运动做出反应。对于大多数这些最初没有反应的单位，在发炎的膝盖中可以检测到感受野。这种变化的时间过程与高阈值纤维相似。可以得出结论，高岭土和角叉菜胶引起的急性实验性关节炎导致增强的机械敏感性在各种类型的关节传入，包括非伤害性以及伤害性和最初无反应的。最早的变化出现在低阈值传入。高阈值单位和无反应单位对温和刺激的反应性主要是在行为实验中注意到痛觉过敏和疼痛的时候发展的。有人建议，疼痛发炎组织的结果，从致敏的高阈值和无反应的传入与可能的贡献，主要是低阈值单位。
In 37 cats anesthetized with .alpha.-chloralose recordings were made from single-afferent units of the medial articular nerve (MAN) of the right knee joint. First the mechanosensitivity of such units was characterized while the joint was in normal condition. Thereafter, keeping the afferents under continuous observation, an experimental arthritis was induced by injecting kaolin and carrageenan into the joint cavity. The effects of the developing arthritis including the time course of the changes were studied on low- and high-threshold units and on afferents that had no mechanosensitivity in the normal joint. The arthritis increased the mechanosensitivity in the majority of the low-threshold units, i.e., in units that responded already in the normal joint to movements in the working range. Enhanced responses to movements were found for 12 of 16 thick myelinated group II, 10 of 10 fine myelinated group III, and 1 of 3 unmyelinated group IV afferents. The augmentation of reactions developed in most cases within the first hour after the injection of the inflammatory compounds, sometimes starting immediately after the injection. A further rise of the mechanosensitivity was observed within the following 2-4 h. In most group III units enhanced responses for movements were accompanied by an induction or increase of resting discharges. In 1 group II and 1 group IV unit spontaneous activity developed in the absence of any change of movement-sensitivity. The inflammation led to enhanced mechanosensitivity in high-threshold afferents, i.e., in units that responded in the normal joint only to noxious movements exceeding the working range of the knee. One group II, 10 of 12 group III, and 5 of 10 group IV units of this type became responsive to movements in the working range during development of arthritis, in most cases within the second to third hour after induction of inflammation with a further increase later on. In a high proportion of these units resting activity was induced too. Few high-threshold units developed spontaneous discharges but no response to movements in the working range. The time course for development of resting activity was similar to that for lowering of the mechanical threshold. The experimental arthritis induced afferent activity in 1 of 2 group III and 10 of 14 group IV units that in the normal joint were unresponsive to local mechanical stimulation and to innocuous/noxious movements (but responsive to a bolus of a KCl-solution applied intraarterially close to the joint). Some fibers started to respond to movements in the working range and developed resting activity, some began to respond only to extreme movements of the inflamed knee. For most of these initially unresponsive units a receptive field became detectable in the inflamed knee. The time course of the changes was similar to that in high-threshold fibers. It is concluded that an acute experimental arthritis induced by kaolin and carrageenan leads to an enhanced mechanosensitivity in various types of articular afferents including nonnociceptive as well as nociceptive and initially unresponsive ones. The earliest changes were found in the low-threshold afferents. Responsiveness of high-threshold and of unresponsive units to gentle stimulation develops mainly at a time in which hyperalgesia and pain are noted in behavioral experiments. It is suggested that pain in inflamed tissue results from sensitized high-threshold and unresponsive afferents with a possible contribution to primarily low-threshold units.