Department of Physiology and Pharmacology, University of Western Ontario, , London, Ontario, Canada.
Philos Trans R Soc Lond B Biol Sci. 2013 Sep 9;368(1628):20130068. doi: 10.1098/rstb.2013.0068. Print 2013 Oct 19.
Several decades of patient, functional imaging and neurophysiological studies have supported a model in which the lateral prefrontal cortex (PFC) acts to suppress unwanted saccades by inhibiting activity in the oculomotor system. However, recent results from combined PFC deactivation and neural recordings of the superior colliculus in monkeys demonstrate that the primary influence of the PFC on the oculomotor system is excitatory, and stands in direct contradiction to the inhibitory model of PFC function. Although erroneous saccades towards a visual stimulus are commonly labelled reflexive in patients with PFC damage or dysfunction, the latencies of most of these saccades are outside of the range of express saccades, which are triggered directly by the visual stimulus. Deactivation and pharmacological manipulation studies in monkeys suggest that response errors following PFC damage or dysfunction are not the result of a failure in response suppression but can best be understood in the context of a failure to maintain and implement the proper task set.
几十年来,对患者进行的功能性成像和神经生理学研究支持这样一种模式,即外侧前额叶皮层(PFC)通过抑制眼球运动系统的活动来抑制不想要的眼球运动。然而,最近对猴子进行的 PFC 去激活和上丘神经记录的综合研究结果表明,PFC 对眼球运动系统的主要影响是兴奋性的,这与 PFC 功能的抑制模型直接矛盾。尽管 PFC 损伤或功能障碍患者向视觉刺激的错误眼球运动通常被标记为反射性的,但这些眼球运动的潜伏期大多超出了直接由视觉刺激触发的表达性眼球运动的范围。猴子的去激活和药物操作研究表明,PFC 损伤或功能障碍后的反应错误不是由于反应抑制失败,而是最好在未能维持和执行适当任务集的背景下加以理解。