Nicotinic receptors modulate the onset of reactive oxygen species production and mitochondrial dysfunction evoked by glutamate uptake block in the rat hypoglossal nucleus

详细信息    查看全文

• 作者：Maria Tortora ; Silvia Corsini ; ^{scorsini@sissa.it} ; Andrea Nistri
• 关键词：ACh ; acetylcholine ; ALS ; amyotrophic lateral sclerosis ; DHβE ; dihydro-beta-erythroidine ; DHR 123 ; dihydrorhodamine ; EAATs ; excitatory amino acid transporters ; HMs ; hypoglossal motoneurons ; MLA ; methyllycaconitine ; MTT ; mitochondrial toxicity test ; nAChR ; nicotinic acetylcholine receptor ; Rho 123 ; rhodamine 123 ; ROS ; reactive oxygen species ; TBOA ; DL-threo-beta-benzyloxyaspartate
• 刊名：Neuroscience Letters
• 出版年：2017
• 出版时间：3 February 2017
• 年：2017
• 卷：639
• 期：Complete
• 页码：43-48
• 全文大小：1125 K
• 卷排序：639

文摘

Glutamate uptake block evokes hypoglossal motoneuron damage due to excitotoxicity. Reactive oxygen species are the earliest excitotoxic players for oxidative damage. Mitochondrial energy deficit is manifested later. Intrinsic cholinergic transmission is inadequate to arrest these events. Nicotinic receptor activation by nicotine provides strong neuroprotection.