Scudder Charles A, McGee David M
Department of Otolaryngology, University of Pittsburgh, Pittsburgh, Pennsylvania 15213, USA.
J Neurophysiol. 2003 Aug;90(2):1011-26. doi: 10.1152/jn.00193.2002.
Saccade accuracy is known to be maintained by adaptive mechanisms that progressively reduce any visual error that consistently exists when the saccade ends. We used an experimental paradigm known to induce adaptation of saccade size while monitoring the neural correlates of this adaptation. In rhesus monkeys where the medial and lateral recti of one eye were surgically weakened, patching the unoperated eye and forcing the monkey to use the weakened eye induced a gradual increase in saccade size in both eyes until the viewing, weak eye almost acquired the target in one step. Subsequent patching of the weakened eye gradually reversed the situation, so that the saccades in the viewing, normal eye decreased from an initial overshooting to normal. In the caudal fastigial nuclei of unadapted monkeys, neurons typically exhibit an early burst of spikes that is correlated with the onset of contraversive saccades and a later burst of spikes that is correlated with the termination of ipsiversive saccades. Comparing the discharges of the same fastigial neurons recorded before and during adaptation, this basic pattern did not change, but some parameters of the discharges did. The most consistent changes were in the latency of the burst for ipsiversive saccades, which was positively correlated with saccade size (1.28 ms/deg), and in the number of spikes associated with contraversive saccades, which was also positively correlated (0.55 spikes/deg). The former was more important when saccade size was decreasing, and the latter was more important when saccade size was increasing. Based on current knowledge of the anatomical connections of fastigial neurons, as well as on the effects of cerebellar lesions and on recordings in other structures, we argue that these changes are appropriate for causing the associated changes in saccade size.
已知扫视准确性是由适应性机制维持的,这种机制会逐渐减少扫视结束时持续存在的任何视觉误差。我们使用了一种已知可诱导扫视大小适应性变化的实验范式,同时监测这种适应性变化的神经关联。在恒河猴中,通过手术削弱一只眼睛的内直肌和外直肌,遮盖未手术的眼睛并迫使猴子使用被削弱的眼睛,会导致两只眼睛的扫视大小逐渐增加,直到注视时,较弱的眼睛几乎能一步到位地对准目标。随后遮盖较弱的眼睛会逐渐扭转这种情况,使得注视时正常眼睛的扫视从最初的过冲减小到正常。在未适应的猴子的尾侧顶核中,神经元通常会出现与对侧扫视开始相关的早期尖峰爆发,以及与同侧扫视终止相关的后期尖峰爆发。比较适应前和适应过程中记录的同一顶核神经元的放电情况,这种基本模式没有改变,但放电的一些参数发生了变化。最一致的变化是同侧扫视爆发的潜伏期,它与扫视大小呈正相关(1.28毫秒/度),以及与对侧扫视相关的尖峰数量,也呈正相关(0.55个尖峰/度)。当扫视大小减小时,前者更重要;当扫视大小增加时,后者更重要。基于目前对顶核神经元解剖连接的了解,以及小脑损伤的影响和其他结构的记录,我们认为这些变化适合引起扫视大小的相关变化。