| Project/Area Number |
16300129
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neurophysiology and muscle physiology
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| Research Institution | University of Tsukuba |
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Principal Investigator |
YOSHIDA Kaoru University of Tsukuba, Graduate School of Comprehensive Human Sciences, Professor, 大学院人間総合科学研究科, 教授 (50111373)
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| Co-Investigator(Kenkyū-buntansha) |
IWAMOTO Yoshiki University of Tsukuba, Graduate School of Comprehensive Human Sciences, Associate Professor, 大学院人間総合科学研究科, 助教授 (50184908)
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| Project Period (FY) |
2004 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥11,700,000 (Direct Cost: ¥11,700,000)
Fiscal Year 2006: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2005: ¥4,600,000 (Direct Cost: ¥4,600,000)
Fiscal Year 2004: ¥5,700,000 (Direct Cost: ¥5,700,000)
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| Keywords | saccade / burst neuron / omnipause neuron / glycinergic inhibition / iontophoresis / adaptation / error signal / microstimulation / グレシン抑制 / 運動学習 / 適応 / 眼振急速相 / ボーズニューロン / グリシン抑制 / 学習捉通 / 小脳 / 眼振 / 緩徐相 / 急速相 / GABA / グリシン / 抑制遮断 / 前庭神経核 |
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| Research Abstract |
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
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