1998 Fiscal Year Final Research Report Summary
Saccade-related inputs to the saccade generator : an intracellular study in alert cats
| Project/Area Number |
09680811
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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 |
神経・脳内生理学
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| Research Institution | University of Tsukuba |
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Principal Investigator |
YOSHIDA Kaoru Inst.Basic Med.Sci., Dept.Physiol., University of Tsukuba Professor, 基礎医学系, 教授 (50111373)
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| Project Period (FY) |
1997 – 1998
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| Keywords | saccade / pause neuron / burst neuron / IPSPs / velocity input |
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| Research Abstract |
Omnipause neurons (OPNs) are midline pontine neurons that are thought to control a number of oculomotor behaviors, especially saccades. Intracellular recordings were made from OPNs in alert cats to elucidate saccade-associated postsynaptic events and thereby determine what patterns of afferent discharge impinge upon OPNs to cause their saccadic inhibition. The membrane potential of OPNs exhibited steep hyperpolarization before each saccade which lasted for the whole period of the saccade. The hyperpolarization was reversed to depolarization by intracellular injection of C1- ions, indicating it consisted of inhibitory postsynaptic potentials (IPSPs). The duration of the hyperpolarization was almost equal to the duration of the saccades. The time course of the hyperpolarization was similar to that of the radial eye velocity except for the initial phase. During the falling phase of eye velocity, the correlation between the instantaneous amplitude of hyperpolarization and the instantaneous
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eye velocity was highly significant. The amplitude of hyperpolarization at the eye velocity peak was significantly correlated with the peak eye velocity. The time integral of the hyperpolarization was correlated with the amplitude of saccades. The initial phase disparity between the hyperpolarization and eye velocity was due to the relative constancy of peak time of the initial steep hyperpolarization regardless of the later potential profile that covaried with the eye velocity. The hyperpolarization led the beginning of saccades by 16 ms, which is longer than the lead time for medium-lesd burst neurons. These results demonstrate that the pause of activity in OPNs is caused by LPSPs initiated by an abrupt, intense input and maintained, for the whole duration of saccade, by afferents conveying eye velocity signals. We suggest that the initial sudden inhibition originates from central structures such as the superior colliculus and that the eye velocity-related inhibition originates from the burst generator in the brain stem. Less
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