Suppression mechanisms of brainstem saccade generator by the caudal superior colliculus - Neural mechanisms of visual fixation -
| Project/Area Number |
17500271
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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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 | Tokyo Medical and Dental University |
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Principal Investigator |
SUGIUCHI Yuriko Tokyo Medical and Dental University, Graduate School, Lecturer, 大学院医歯学総合研究科, 講師 (30251523)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2006: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 2005: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | superior colliculus / inhibitory burst neuron / pause neuron / saccade / visual fixation |
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| Research Abstract |
The superior colliculus (SC) controls saccadic eye movement. In the SC, there is a motor map that reflects directions and amplitudes of saccades. Recently, it was proposed that neurons in the rostral SC maybe specifically involved in controlling fixation and suppressing saccades. Therefore, the rostral part of the SC is called the "fixation zone", whereas the remaining caudal part is called the "saccade zone". However, it was also reported that most fixation neurons do not pause for small contraversive saccades, but increase their activity. This finding has led the idea that fixation neurons are only the rostral extension of the saccade-related neurons in the more caudal colliculus. Therefore, the functional independence of the fixation zone in the rostral part has been controversial. In order to analyze the functional independence of the rostral part of the SC, we analyzed the neural connections from the rostral and caudal parts of the SC to inhibitory burst neurons (IBNs) and omnipause neurons (OPNs) using intracellular recording and straining methods in anesthetized cats.
IBNs received monosynaptic excitatory postsynaptic potentials (EPSPs) from the contralateral caudal SC. They received disynaptic inhibitory postsynaptic potentials (IPSPs) from the ipsilateral caudal SC and bilateral rostral SCs. Lesion experiment suggested that the disynaptic IPSPs from the rostral parts of the bilateral SC was mediated by OPNs, and this was confirmed by the electrophysiological evidence. OPNs received monosynaptic EPSPs from the bilateral rostral SCs, and intracellular straining of such neurons showed projection to the contralateral excitatory burst neuron and IBN regions. These results indicate that the rostral of the SC directly activate OPNs and disynaptically inhibit IBNs via OPNs. The different pattern of synaptic input from the rostral and caudal SC to IBNs and OPNs indicated functional difference of the rostral part of the SC from its caudal part.
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Report
(3 results)
Research Products
(23 results)
