Department of Physiology and Biophysics, University of Washington, Seattle, WA 98195-7330, USA.
Brain Res. 2010 Dec 17;1366:93-100. doi: 10.1016/j.brainres.2010.10.027. Epub 2010 Oct 15.
The oculomotor vermis (OMV) of the cerebellum is necessary for the generation of the accurate rapid eye movements called saccades. Large lesions of the midline cerebellar cortex involving the OMV cause saccades to become hypometric and more variable. However, saccades were not examined immediately after these lesions so the interpretation of the resulting deficits might have been contaminated by some adaptation to the saccade dysmetria. Therefore, to better understand the contribution of the OMV to normal saccades, we impaired its operation locally by injecting small amounts of either an agonist or antagonist of γ-aminobutyric acid (GABA), which is a ubiquitous neurotransmitter throughout the cerebellar cortex. Muscimol, a GABA agonist, inactivated part of the OMV, whereas bicuculline, an antagonist, disinhibited it. Muscimol caused all ipsiversive horizontal saccades from 5 to 30° to become hypometric. In contrast, bicuculline produced an amplitude-dependent dysmetria: ipsiversive horizontal saccades elicited by target steps <10° became hypometric, whereas those in response to larger steps became hypermetric. At the transition target amplitude, saccade amplitudes were quite variable with some being hypo- and others hypermetric. After most injections of either agent, saccades had lower peak velocities and longer durations than pre-injection saccades of the same amplitude. The longer durations were associated with a prolongation of the deceleration phase. Both agents produced inconsistent effects on contraversive saccades. These results establish that the oculomotor vermis helps control the characteristics of normal ipsiversive saccades and that GABAergic inhibitory processes are a crucial part of this process.
小脑的动眼神经核(OMV)对于产生称为扫视的准确快速眼球运动是必要的。中线小脑皮层的大病变涉及 OMV 会导致扫视变得小且更可变。然而,这些病变后没有立即进行扫视检查,因此对导致的缺陷的解释可能受到扫视偏距的一些适应的污染。因此,为了更好地理解 OMV 对正常扫视的贡献,我们通过注射少量的γ-氨基丁酸(GABA)激动剂或拮抗剂来局部破坏其功能,GABA 是整个小脑皮层中的一种普遍存在的神经递质。GABA 激动剂毒蕈碱使 OMV 的一部分失活,而拮抗剂印防己毒素则使其去抑制。毒蕈碱使所有 5 到 30°的同侧水平扫视变得小。相比之下,印防己毒素产生了与幅度相关的偏距:小于 10°的目标步引起的同侧水平扫视变得小,而响应较大步的扫视变得大。在过渡目标幅度处,扫视幅度非常可变,有些是小的,有些是大的。在注射这两种药物中的大多数药物后,扫视的峰值速度和持续时间比相同幅度的注射前扫视要低。较长的持续时间与减速阶段的延长有关。两种药物对视交叉扫视的影响不一致。这些结果表明,动眼神经核有助于控制正常同侧扫视的特征,并且 GABA 能抑制过程是该过程的关键部分。