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

本文观察了背柱-丘脑通路参与实验性单神经病大鼠丘脑神经元反应特性的改变。在慢性压迫性神经损伤（CCI）大鼠的丘脑腹后外侧核（VPL）记录了背柱-丘脑通路，并观察了损毁背柱-丘脑通路和应用谷氨酸受体拮抗剂的影响（CNQX，MK 801）对薄束核（GN）的VPL神经元反应特性的影响。从本研究中获得以下结果。1.在损伤研究中，DC和DC+GN损伤后，低阈值机械感受（LTM）和宽动态范围（WDR）神经元对感受野的无害机械刺激的反应显著降低。而DC和DC+GN损伤后CCI对侧VPL核的WDR神经元对伤害性刺激的反应为选择性神经元，明显高于假手术对侧和未损伤的VPL核.在给药研究中，在GN池上应用CNQX后，CCI侧对侧VPL核中WDR神经元对分级机械刺激的诱发反应呈剂量依赖性地被抑制。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降低。提示DC通路可能在机械性痛敏的发生中起重要作用。

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.