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通过微刺激猴子小脑后蚓部诱发扫视性眼球运动时浦肯野细胞的参与。

Involvement of Purkinje cells in evoking saccadic eye movements by microstimulation of the posterior cerebellar vermis of monkeys.

作者信息

Noda H, Fujikado T

出版信息

J Neurophysiol. 1987 May;57(5):1247-61. doi: 10.1152/jn.1987.57.5.1247.

Abstract

Neural mechanisms for evoking saccadic eye movements by microstimulation of the posterior vermis were investigated in monkeys trained to fixate a visual target. The low-threshold region from which saccadic eye movements could be evoked with currents less than 10 microA was confined to lobule VII in two monkeys and it included a posterior part of lobule VI (lobule VIc) in another monkey. The region from which saccade-related neural activity was recordable coincided with the low-threshold region. This region corresponded to the vermal lobules from which eye position and saccade-related Purkinje cells were recorded. Kainic acid (kainate) injected in the white matter of lobule VII resulted in severe losses of Purkinje cells within a radius of 1-2 mm of the injection site. The lesion tended to be larger toward the peripheral cerebellar cortices, which were connected to the injection site by natural courses of the afferent and efferent fibers. After the kainate administration, the distribution of saccade-related neural activity did not differ significantly from that of the preoperative mapping, in spite of the severe losses of cortical neurons. Burst discharges of mossy fibers were recordable in the white matter near the injection site, indicating that afferent fibers were relatively unaffected by kainate. After kainate administration, the saccadic eye movements could no longer be evoked by microstimulation applied to the posterior vermis. The stimulus sites from which saccades could be evoked after kainate administration were always associated with the presence of intact Purkinje cells. In such cases, the minimum current necessary to evoke saccades depended on the percentages of intact Purkinje cells spared. In the folia with normal Purkinje cell layers, the amplitude and direction of evoked saccades and the thresholds for evoking such eye movements were almost comparable to the preoperative data. Saccadic eye movements in response to microstimulation of the posterior vermis were caused by orthodromic impulses conveyed through the axons of the Purkinje cells. Insofar as the saccades elicited from lobule VII with currents less than 10 microA are concerned, antidromic activation of the afferent fibers is not the neural mechanisms subserving the oculomotor responses.

摘要

在经过训练能注视视觉目标的猴子身上,研究了通过微刺激小脑后叶蚓部诱发眼球跳动性眼动的神经机制。在两只猴子中,用小于10微安的电流就能诱发眼球跳动性眼动的低阈值区域局限于小叶VII,而在另一只猴子中,该区域包括小叶VI的后部(小叶VIc)。可记录到与眼球跳动相关神经活动的区域与低阈值区域重合。该区域对应于记录到眼位和与眼球跳动相关的浦肯野细胞的蚓部小叶。向小叶VII的白质注射海人酸会导致注射部位半径1 - 2毫米范围内的浦肯野细胞严重缺失。损伤在向周边小脑皮质方向往往更大,周边小脑皮质通过传入和传出纤维的自然路径与注射部位相连。注射海人酸后,尽管皮质神经元严重缺失,但与眼球跳动相关的神经活动分布与术前测绘结果相比无显著差异。在注射部位附近的白质中可记录到苔藓纤维的爆发性放电,表明传入纤维相对未受海人酸影响。注射海人酸后,施加于小脑后叶蚓部的微刺激不再能诱发眼球跳动性眼动。海人酸注射后能诱发眼球跳动的刺激部位总是与完整浦肯野细胞的存在相关。在这种情况下,诱发眼球跳动所需的最小电流取决于 spared 完整浦肯野细胞的百分比。在浦肯野细胞层正常的小叶中,诱发眼球跳动的幅度、方向以及诱发此类眼动的阈值与术前数据几乎相当。对小脑后叶蚓部微刺激产生的眼球跳动性眼动是由通过浦肯野细胞轴突传导的顺行冲动引起的。就用小于10微安电流从小叶VII诱发的眼球跳动而言,传入纤维的逆向激活不是支持动眼反应的神经机制。

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