1998 Fiscal Year Final Research Report Summary
Alteration of NMDA Response by Neuronal Injury
| Project/Area Number |
09670046
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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 |
General physiology
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| Research Institution | KYUSHU UNIVERSITY |
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Principal Investigator |
NABEKURA Junichi Kyushu University Associate Professor, 医学部, 助教授 (50237583)
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| Co-Investigator(Kenkyū-buntansha) |
NODA Mami Kyushu University Assistant Professor, 医学部, 助手 (80127985)
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| Project Period (FY) |
1997 – 1998
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| Keywords | Neuron / Injury / Receptor / transmitter / Glutamate / NMDA |
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| Research Abstract |
N-methyl-D-aspartate (NMDA) receptors play important roles in neural development, neuronal degeneration, neuronal regeneration and synaptic plasticity. One of most important characteristics of NMDA receptor-response is voltage dependent block of this channel by extracellular Mg^<2+> as well as its high Ca^<2+> permeability. Post traumatic change of the voltage-dependent Mg^<2+> block of NMDA-induced response was investigated on the dorsal motor nucleus of vagus (DMV) neurons freshly dissociated from the rats receiving the vagaI nerve crush at the neck in vivo at hours to 10 days before making preparations. The reduction of voltage dependent Mg^<2+> block of NMDA response became evident at at least 12 hours after the injury, sustained until 5 days and recovered within 10 days. The Mg^<2+> block was not affected by the local application of colchicine onto the vagal axon, suggesting that the neuronal trauma such as axonal crush, not the blockade of the axonal flow, is responsible for the change of the sensitivity of NMDA response to extracellular Mg^<2+>. In addition, reduction of Mg^<2+> block by the nerve injury persisted in the applications of PKC modulators, such as staurosporine, chelerythrine and calphostin C, suggesting that increase of PKC activity after axonaI injury is not involved in this change.
The NMDA receptor response was also less sensitive to Mg^<2+> in immature animals. in this sense, injured DMV neurons re-acquired immature characteristics regarding the sensitivity to extracellular Mg^<2+>.
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