1994 Fiscal Year Final Research Report Summary
STUDIES ON THE IMPROVEMENT OF EQUILIBRIUM FUNCTIONS
| Project/Area Number |
04671034
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Otorhinolaryngology
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| Research Institution | GIFU UNIVERSITY |
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Principal Investigator |
MIYATA Hideo Gifu University School of Medicine, Professor., 医学部, 教授 (90021469)
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| Co-Investigator(Kenkyū-buntansha) |
MIZUTA Keisuke Gifu University School of Medicine, Assistant Professor., 医学部付属・病院, 講師 (10190638)
ITO Yatsuji Gifu University School of Medicine, Assistant Professor., 医学部付属・病院, 講師 (60135192)
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| Project Period (FY) |
1992 – 1994
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| Keywords | Pigmented rabbits / Optokinetic training / Optokinetic nystagmus / NMDA receptors / MK-801 / Oculomotor pathway / Rotatory training / Methamphetamine |
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| Research Abstract |
To evaluate a neural mechanism and neurotransmitters linked with the optokinetic training (OKT) - induced improvement of optokinetic nystagmus (OKN), we examined the effect of OKT on OKN in pigmented rabbits. The animals received OKT for 3 weeks and the OKN was tested with a step stimulus using the OKN drum (a type of Ohm). Since the OKN is affected by the state of alertness in animals, we also examined the effect of methamphetamine (MAP) on the OKN.MAP reduced the time to the steady state in OKN,but did not change either the average steady state gain or the duration of optokinetic after-nystagmus (OKAN). OKT significantly increased the average steady state gain, but did not change either the time to the steady state or the duratin of OKAN.These results suggested that the oculomotor pathway associated with the pursuit mechanism, except for the velocity storage mechanism, may be responsible for the improvement of OKN by OKT.
To investigate the involvement of N-methyl-D-aspartic and (NMDA) receptors in the improvement of OKN by OKT,we examined the effect on the optokinetic reflex of MK-801 ((]SY.+-。[)-5-methyl-10,11-dihydro-5H-dibenzo [a, d] cyclohepten-5,10-imine maleate). The pigmented rabbits, in which OKN had been improved by OKT for 12 days, were injected with the MK-801 and then their OKN were blocked ; the blockade was completely reversed with 72 hrs. At intoxic doses (less than 0.1 mg/kg), this drug caused a reduction of OKN,but did not influenced the post-rotatory nystagmus (PRN), locomotor activity nor the electroencephalogram of the cerebral cortex and hippocampus. Therefore we suggested that the activation of the NMDA receptors in the oculomotor pathway may be involved in the improvement of OKN by OKT.
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