Role of inhibition in adaptation of vestibular and saccadic eye movements.

前庭和扫视眼球运动的准确性由运动学习机制维持。我们研究了1)抑制在参与这些眼动的运动前通路中的作用，以及2)传递错误信号以进行扫视适应的通路。使用多层微电极，我们记录了前庭核和脑桥网状结构细胞的单个单位活动，并电泳法应用GABA受体拮抗剂或甘氨酸受体拮抗剂。在应用GABA拮抗剂后，水平管相关的前庭二级神经元对头部旋转的反应显著增加。对反应期的分析表明，这些神经元接受了非连合来源的GABA能输入，很可能是来自小叶。另一方面，甘氨酸能抑制在眼跳指令的产生中起关键作用。因此，到达更年期神经元的抑制性触发和闩锁信号都是由甘氨酸…介导的。更多的感觉神经传入。从全食神经元到运动前爆发神经元的抑制也是甘氨酸能的，并被发现是抑制视觉反应所必需的。我们在单个实验中考察了重复的眼跳适应的影响。分析表明，在恢复过程中，对以前学习的记忆仍然存在，并有助于随后的适应。这种记忆不会仅仅随着时间的推移而消失，而是通过重复的零错误动作来主动擦除。结果表明，眼跳系统具有多个可塑性过程，错误信号对运动学习具有重要作用。然而，关于传递错误信号以进行眼跳适应的通路，我们知之甚少。我们发现，眼跳后对中脑被盖的微刺激会在眼跳增益中产生逐渐而显著的变化。产生的变化的时间和空间特征与真实视觉错误引起的适应相似。我们得出的结论是，微刺激产生了强大的学习信号，这些信号决定了眼跳终点的适应性转移的方向。较少

The accuracy of vestibular and saccadic eye movements is maintained by motor learning mechanisms. We examined 1) a role of inhibition in the premotor pathways participating in these eye movements, and 2) the pathways mediating error signals for saccadic adaptation.Using a multibarel microelectrode, we recorded single unit activity from cells in the vestibular nucleus and pontine reticular formation, and iontophoretically applied GABA receptor antagonists or glycine receptor antagonist. Following application of GABA antagonists, horizontal canal-related secondary vestibular neurons showed a marked increase in the gain of their response to head rotation. Analysis of the response phase suggested that these neurons received GABAergic input of non-commissural origin, most likely from the flocculus. On the other hand, glycinergic inhibition played critical roles in generation of saccadic command. Thus, both the inhibitory trigger and latch signals to omnipause neurons were mediated by glycin … More ergic afferents. Inhibition from omnipause neurons to premotor burst neurons was also glycinergic and found to be necessary to suppress visual responses.We examined effects of repetition of saccadic adaptation during single experiments. Analyses revealed that a memory of previous learning remains during recovery and facilitates subsequent adaptation. This memory does not disappear merely with time but is erased actively by repeated zero-error movements. Results suggest that the saccadic system is equipped with more than one plasticity process.Error signals are vital to motor learning. However, little is known about pathways that transmit error signals for saccadic adaptation. We found that microstimulation of the midbrain tegmentum following saccades produces gradual and marked changes in saccade gain. The spatial and temporal characteristics of the produced changes were similar to those of adaptation induced by real visual error. We conclude that microstimulation created powerful learning signals that dictate the direction of adaptive shift in saccade endpoints. Less