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Oculomotor System

開催日 2014/9/11
時間 17:00 - 18:00
会場 Room H(304)
Chairperson(s) 杉内 友理子 / Yuriko Sugiuchi (東京医科歯科大学医歯学総合研究科システム神経生理学 / Department of Systems Neurophysiology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Japan)
伊澤 佳子 / Yoshiko Izawa (東京医科歯科大学大学院医歯学総合研究科 システム神経生理学 / Department of Systems Neurophysiology, Tokyo Medical and Dental University, Japan)

Anti-saccade signals in the primate cerebellar dentate nucleus

  • O1-H-5-3
  • 國松 淳 / Jun Kunimatsu:1 鈴木 智貴 / Tomoki Suzuki:1 田中 真樹 / Masaki Tanaka:1 
  • 1:北海道大学 / Dept. of Physiology, Hokkaido Univ. School of Medicine, Sapporo, Japan 

The anti-saccade task has been used to investigate the neural mechanisms of volitional oculomotor control. In this task, subjects are required to make a saccade to an unmarked location opposite to a flashed stimulus. Because the lateral cerebellum is known to be involved in the voluntary control of somatic movements, it may also contribute to the generation of anti-saccades. Indeed, recent imaging studies have revealed the enhanced activity in the cerebellum during anti-saccades (Tu et al., 2006; Jamadar et al., 2013). To investigate the role of the cerebellum, we recorded from single neurons in the cerebellar dentate nucleus in monkeys performing anti-saccades, and examined the effects of local inactivation.
Among 28 task-related neurons, more than one third showed greater activity during anti-saccades than during reflexive saccades. In the population as a whole, neuronal activity in the dentate nucleus was significantly greater during anti-saccades. Because the enhanced activity disappeared in erroneous anti-saccade trials, these signals might play a role in suppressing reflexive saccades to the flashed stimulus. To examine the causal role, the recording sites were locally inactivated by injecting a small amount of muscimol (5 µg in 1 µl) in separate experiments. For all 3 sites tested so far, the number of erroneous saccades increased significantly in the anti-saccade trials in either or both directions. Furthermore, the latency of saccades was also altered during inactivation; one site delayed, while the other two sites shortened anti-saccade latency.
Our results show that signals in the cerebellar dentate nucleus do play roles in the generation of anti-saccades. These signals may be sent to the prefrontal cortex or to the basal ganglia via the thalamus. The neuronal processes in the lateral cerebellum through the dentate nucleus to the frontal cortices might be essential for the proactive control of volitional eye movements.

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