Response properties of thalamic neurons in the rats with experimental mononeuropathy -the role of the dorsal column -thalamic pathway-

我们从慢性压迫性神经损伤(CCI)大鼠丘脑腹后外侧核(VPL)观察了背柱-丘脑通路参与改变实验性单神经病大鼠丘脑神经元的反应特性，并观察了损毁背柱-丘脑通路和向薄层核(GN)注射谷氨酸受体拮抗剂(CNQX、MK801)对VPL神经元反应特性的影响。本研究取得了以下研究结果：1.在损伤研究中，DC和DC GN损伤后，低阈值机械感受性(LTM)和宽动态范围(WDR)神经元对无害性机械刺激对感受野的反应显著降低。结果：1.损毁DC和DC GN后，WDR神经元对伤害性刺激的反应在CCI侧对侧的VPL核中为选择性的，高于假手术侧和未损毁侧的VPL核。在给药研究中，GN池给予CNQX后，CCI侧对侧VPL核WDR神经元对机械刺激的诱发反应呈剂量依赖性抑制。应用MK-801后，CCI对侧VPL核WDR神经元对伤害性刺激和背景活动的诱发反应呈剂量依赖性抑制。提示DC通路在机械性痛觉过敏的发生发展中可能起重要作用。

We examined the involvement of the dorsal column-thalamic pathway in changes the response properties of thalamic neurons in the rats with experimental mononeuropathy We recorded from the ventro-postero-lateral nucleus of thalamus (VPL) in rats with chronic constriction nerve injury (CCI), and examined the effects of the lesion of the dorsal column (DC) -thalamic pathway and the administration of the glutamate receptor antagonists (CNQX, MK801) to the gracile nucleus (GN) on the response properties of VPL neurons. The following results were obtained from this study.1. In the lesion study, responses of low threshold mechanoreceptive (LTM) and wide dynamic range (WDR) neurons to innocuous mechanical stimulation to the receptive fields were significantly decreased after DC and DC+GN lesions. However, the responses of WDR neurons to noxious stimuli were selectrons in the VPL nucleus contralateral to CCI side after DC and DC+GN lesions was grater than that in the VPL nucleus contralatral to the sham operated side and naive.2. In the administration study, the evoked responses of WDR neuron, in the VPL nucleus contralateral to CCI side, to the graded mechanical stimulation were dose-dependently depressed after application of CNQX on GN pool. The evoked responses of WDR neuron, in the VPL nucleus contralateral to CCI side, to the noxious stimulation and background activity were dose-dependently depressed after application of MK-801.We suggested that DC-pathway might take an important role in the development of mechanical hyperalgesia.