Stimulation of nicotinic acetylcholine receptors protects motor neurons
Stimulation of nicotinic acetylcholine receptors protects motor neurons
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DOI：
10.1016/j.bbrc.2005.03.115
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发表时间：
2005-05-20
影响因子：
3.1
通讯作者：
Shimohama, S
中科院分区：
文献类型：
--
作者：
Nakamizo, T;Kawamata, J;Shimohama, S
本研究表明，尼古丁的管理，防止谷氨酸诱导的运动神经元死亡的原代培养的大鼠螺旋索。尼古丁诱导的神经保护作用被二氢-β-赤藓环素（DHPE）或α-银环蛇毒素（α BT）抑制，表明其通过α 4 β 2和α 7烟碱乙酰胆碱受体（nAChR）介导。通过免疫组织化学方法在大鼠脊髓运动神经元上鉴定α 4 β 2和α 7 nAChRs。我们还证明，加兰他敏，乙酰胆碱酯酶抑制剂与变构nAChR增强配体的属性，防止谷氨酸诱导的运动神经元死亡。这些结果表明，nAChR的刺激可用作ALS的治疗。(c)2005年爱思唯尔公司All rights reserved.
The present study demonstrated that administration of nicotine prevented glutamate-induced motor neuronal death in primary cultures of the rat spiral cord. The nicotine-induced neuroprotection was inhibited by either dihydro-beta-erythroidin (DHPE) or alpha-bungarotoxin (alpha BT), suggesting that it is mediated through both alpha 4 beta 2 and alpha 7 nicotinic acetylcholine receptors (nAChRs). Both alpha 4 beta 2 and alpha 7 nAChRs were identified on rat spinal motor neurons by immunohistochemical methods. We also demonstrated that galantamine, an acetylcholinesterase inhibitor with allosteric nAChR-potentiating ligand properties, prevented glutamate-induced motor neuronal death. These results suggest that stimulation of nAChR may be used as a treatment for ALS. (c) 2005 Elsevier Inc. All rights reserved.