この研究は、培養されたラット海馬ニューロンのN-メチル-D-アスパラギン酸（NMDA）受容体チャンネルに対する静磁界ばく露の影響を調べた。NMDA受容体拮抗薬ジゾシルピン（MK-801）とともに8日間培養したラット海馬ニューロンでは、微小管関連タンパク質2（MAP-2）、脳由来神経栄養因子（BDNF）および成長関連タンパク質43（GAP-43）の両方のmRNAの有意な発現低下が見られ、かつ生存率も低下した。MK-801は、NMDA受容体のNR1サブユニットの発現を低下させるだけでなく、NR2Bの発現に影響を与えることなくNR2Aの発現を増加させた。100 mTの静磁界への15分間ばく露を毎日１回、培養ニューロンに反復的に与えた場合、細胞生存率やニューロン核（NeuN）およびGAP-43の発現に大きな影響を与えることなく、MAP-2の発現が低下した。しかし、MK-801の存在下で培養されたニューロンに同じ静磁界の反復的ばく露を与えた場合、NR1発現を変化させることなく、BDNF mRNAおよびMAP-2の両方の低下が阻止され、加えてNR2Aサブユニットの発現を増加させた。以上の知見は、反復的静磁界ばく露が、培養ラット海馬ニューロンにおける特定のNMDA受容体サブユニットの発現の調節を通じて、MK-801の神経毒性を少なくとも部分的に中和する可能性があることを示唆する、と報告している。
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To evaluate possible protective properties of repetitive daily exposure to static magnetic fields against the neurotoxicity of sustained blockade of N-methyl-D-aspartate (NMDA) receptor channels by dizocilpine (MK-801) in cultured rat hippocampal neurons.
The NMDA receptor antagonist MK-801 was added into culture medium at a concentration of 1-100 µM in hippocampal neurons cultured for up to 8 days in vitro.
Sustained exposure to static magnetic fields modulates cellular maturation and development, at least in part through the up-regulation of NMDA receptor channels.
| 周波数 |
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| タイプ |
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| ばく露時間 | repeated daily exposure, 15 min/day for 8 consecutive days |
| ばく露の発生源／構造 |
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| ばく露装置の詳細 | ferrite magnets with N pole upwards were placed on both sides of the culture dishes which were located at the center of the magnetic fields at a distance of 10 cm from each other. Control dishes were treated under the same environmental conditions as for the exposure groups in the absence of ferrite magnets. |
| 測定量 | 値 | 種別 | Method | Mass | 備考 |
|---|---|---|---|---|---|
| 磁束密度 | 100 mT | - | 測定値 | - | - |
| 周波数 |
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| タイプ |
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| ばく露時間 | continuous for 3 days |
| ばく露の発生源／構造 |
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| 測定量 | 値 | 種別 | Method | Mass | 備考 |
|---|---|---|---|---|---|
| 磁束密度 | 100 mT | - | 測定値 | - | - |
In hippocampal neuronal cultures treated with MK-801 a significant decrease was found in the expression of MAP2 (a major component of cross-bridges between microtubules in dendrites) as well as mRNA for both BDNF and GAP43 (a marker of neuronal maturity that is associated with neuronal development, axonal regeneration, and synaptogenesis). Additionally, a decreased viability was observed. MK-801 not only decreased the expression of the NR1 subunit of NMDA receptors, but also increased NR2A expression, without affecting NR2B expression.
Repetitive daily exposure to static magnetic fields led to a decrease in the expression of MAP2 (to approximately 50% of the control), without significantly affecting cell viability or the expression of neuronal nuclei and GAP43.
However, the exposure to repetitive magnetism prevented decreases in both BDNF mRNA and MAP2. In addition it increased the expression of NR2A subunit, without altering NR1 expression in neurons cultured in the presence of MK-801.
These data suggest that repetitive magnetism may at least in part counteract the neurotoxicity of MK-801 through modulation of the expression of particular NMDA receptor subunits in cultured rat hippocampal neurons.
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