Arts M P, De Zeeuw C I, Lips J, Rosbak E, Simpson J I
Department of Physiology and Neuroscience, New York University School of Medicine, New York, New York 10016, USA.
J Neurophysiol. 2000 Nov;84(5):2552-63. doi: 10.1152/jn.2000.84.5.2552.
The caudal dorsal cap (dc) of the inferior olive is involved in the control of horizontal compensatory eye movements. It provides those climbing fibers to the vestibulocerebellum that modulate optimally to optokinetic stimulation about the vertical axis. This modulation is mediated at least in part via an excitatory input to the caudal dc from the pretectal nucleus of the optic tract and the dorsal terminal nucleus of the accessory optic system. In addition, the caudal dc receives a substantial GABAergic input from the nucleus prepositus hypoglossi (NPH). To investigate the possible contribution of this bilateral inhibitory projection to the visual responsiveness of caudal dc neurons, we recorded the climbing fiber activity (i.e., complex spikes) of vertical axis Purkinje cells in the flocculus of anesthetized rabbits before and after ablative lesions of the NPH. When the NPH ipsilateral to the recorded flocculus was lesioned, the spontaneous complex spike firing frequency did not change significantly; but when both NPHs were lesioned, the spontaneous complex spike firing frequency increased significantly. When only the contralateral NPH was lesioned, the spontaneous complex spike firing frequency decreased significantly. Neither unilateral nor bilateral lesions had a significant influence on the depth of complex spike modulation during constant velocity optokinetic stimulation or on the transient continuation of complex spike modulation that occurred when the constant velocity optokinetic stimulation stopped. The effects of the lesions on the spontaneous complex spike firing frequency could not be explained when only the projections from the NPH to the inferior olive were considered. Therefore we investigated at the electron microscopic level the nature of the commissural connection between the two NPHs. The terminals of this projection were found to be predominantly GABAergic and to terminate in part on GABAergic neurons. When this inhibitory commissural connection is taken into consideration, then the effects of NPH lesions on the spontaneous firing frequency of floccular complex spikes are qualitatively explicable in terms of relative weighting of the commissural and caudal dc projections of the NPH. In summary, we conclude that in the anesthetized rabbit the inhibitory projection of the NPH to the caudal dc influences the spontaneous firing frequency of floccular complex spikes but not their modulation by optokinetic stimulation.
下橄榄核的尾侧背帽（dc）参与水平代偿性眼球运动的控制。它为前庭小脑提供那些对围绕垂直轴的视动刺激进行最佳调节的攀爬纤维。这种调节至少部分是通过视束的顶盖前核和辅助视系统的背侧终核向尾侧dc的兴奋性输入介导的。此外，尾侧dc从舌下前置核（NPH）接受大量的GABA能输入。为了研究这种双侧抑制性投射对尾侧dc神经元视觉反应性的可能贡献，我们在麻醉兔的绒球中记录了垂直轴浦肯野细胞的攀爬纤维活动（即复合动作电位），记录时间为NPH切除性损伤前后。当记录绒球同侧的NPH受损时，自发复合动作电位发放频率没有显著变化；但当双侧NPH都受损时，自发复合动作电位发放频率显著增加。当仅对侧NPH受损时，自发复合动作电位发放频率显著降低。单侧或双侧损伤对匀速视动刺激期间复合动作电位调制的深度或匀速视动刺激停止时复合动作电位调制的短暂持续均无显著影响。仅考虑从NPH到下橄榄核的投射时，损伤对自发复合动作电位发放频率的影响无法解释。因此，我们在电子显微镜水平研究了两个NPH之间连合连接的性质。发现该投射的终末主要是GABA能的，并部分终止于GABA能神经元。考虑到这种抑制性连合连接后，NPH损伤对绒球复合动作电位自发发放频率的影响就NPH的连合和尾侧dc投射的相对权重而言在性质上是可以解释的。总之，我们得出结论，在麻醉兔中，NPH对尾侧dc的抑制性投射影响绒球复合动作电位的自发发放频率，但不影响其对视动刺激的调制。
