2006 Fiscal Year Final Research Report Summary
Ischemic neuronal dysfunction in the vestibular nucleus and plasticity
| Project/Area Number |
16591723
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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 |
Otorhinolaryngology
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| Research Institution | Nara Medical University |
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Principal Investigator |
YAMANAKA Toshiaki Nara Medical University, School of Medicine, Senior Lecturer, 医学部, 講師 (90271204)
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| Co-Investigator(Kenkyū-buntansha) |
OKAMOTO Hideyuki Nara Medical University, School of Medicine, Lecturer, 医学部, 助手 (80316075)
MURAI Takayuki Nara Medical University, School of Medicine, Lecturer, 医学部, 助手 (20326325)
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| Project Period (FY) |
2004 – 2006
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| Keywords | vestibular nucleus / hypoxic depolarization / plasticity / glutamate |
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| Research Abstract |
Brainstem hypoxia due to vertebrobasilar insufficiency is well known to induce vertigo which is caused by an imbalance between the bilateral vestibular nuclei. Electrophysiological studies have been performed to examine the effects of hypoxia on medial vestibular nucleus (MVN).
We previously figured out that the enhancement of neuronal activity (Post Hypoxic Potentiation : PHP) take place in medial vestibular nucleus (MVN) after hypoxia which cause hypoxic depolarization (HD) followed by neuronal dysfunction. In this study, we examined the role of glutamate in the PHP of MVN neuron. Single neuronal activities of MVN in α-chloralose-anesthetized cats were recorded extracellularly with a glass-insulated silver wire microelectrode attached along a several-barreled micropipette. Each barrel was filled with DNQX, non-NMDA glutamate receptor antagonist and MK-801, NMDA glutamate receptor antagonist. These chemicals were applied microiontophoretically to the immediate vicinity of the target neurons. Neuronal firings decreased by 5% O_2 for 3 min, recovered gradually after the termination of hypoxia and showed the increase in firings more than 150% of control about 30 min after hypoxia. This PHP was dependent on the activation of HD and was inhibited by iontophoretic application of DNQX or MK-801 during hypoxia. These results suggest that NMDA and non-NMDA glutamate receptor in MVN is implicated in the production of PHP.
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