title: Effects of Abeta1-42 on the subunits of KATP expression in cultured primary rat basal forebrain neurons.
abstract: ATP-sensitive potassium channels (KATP) play a crucial role in coupling metabolic energy to the membrane potential of cells, thereby functioning as cellular "metabolic sensors." Recent evidence has showed a connection between the amyloid neurotoxic cascade and metabolic impairment. With regard to their neuroprotection in other neuronal preparations, KATP channels may mediate a potential neuroprotective role in Alzheimer's disease (AD). To investigate the effects of Abeta1-42 on the subunits of KATP expression in cultured primary rat basal forebrain cholinergic neurons, primary rat basal forebrain neurons were cultured and evaluated. The subunits of KATP: Kir6.1, Kir6.2, SUR1 and SUR2 expressing changes were observed by double immunofluorescence and immunoblotting when the neurons were exposed to Abeta1-42(2 microM) for different time (0, 24, 72 h). We found a significant increase in the expression of Kir6.1 and SUR2 in the cultured neurons being exposed to Abeta1-42 for 24 h, while Kir6.2 and SUR1 showed no significant change. However, after being treated with Abeta1-42 for 72 h, the expression of the four subunits was all increased significantly compared with the control. These findings suggest that being exposed to Abeta1-42 for different time (24 and 72 h) induces differential regulations of KATP subunits expression in cultured primary rat basal forebrain cholinergic neurons. The change in composition of KATP may contribute to resist the toxicity of Abeta1-42.
authors.affiliation: Department of Neurology, Provincial Hospital affiliated to Shandong University, No. 324 Jingwu Weiqi Road, Jinan 250021, Shandong, PR. China. maguozhao@yahoo.com.cn
authors.forename: Guozhao
authors.initials: G
authors.lastname: Ma
authors.forename: Qingxi
authors.initials: Q
authors.lastname: Fu
authors.forename: Yong
authors.initials: Y
authors.lastname: Zhang
authors.forename: Jianxin
authors.initials: J
authors.lastname: Gao
authors.forename: Jinjiao
authors.initials: J
authors.lastname: Jiang
authors.forename: Ailing
authors.initials: A
authors.lastname: Bi
authors.forename: Kejing
authors.initials: K
authors.lastname: Liu
authors.forename: Yifeng
authors.initials: Y
authors.lastname: Du
authors.forename: Chunfu
authors.initials: C
authors.lastname: Chen
authors.forename: Yuanxiao
authors.initials: Y
authors.lastname: Cui
authors.forename: Lin
authors.initials: L
authors.lastname: Lu
mesh_terms: D016229:Amyloid beta-Peptides / Q000494:pharmacology*; D000818:Animals; D015153:Blotting, Western; D002478:Cells, Cultured; D005260:Female; D019084:Fluorescent Antibody Technique, Indirect; D007150:Immunohistochemistry; D007202:Indicators and Reagents; D054086:KATP Channels / Q000096:biosynthesis* / Q000235:genetics; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D010275:Parasympathetic Nervous System / Q000166:cytology / Q000187:drug effects; D010446:Peptide Fragments / Q000494:pharmacology*; D011247:Pregnancy; D016548:Prosencephalon / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D051381:Rats
chemical_list: D016229:Amyloid beta-Peptides; D007202:Indicators and Reagents; D054086:KATP Channels; D010446:Peptide Fragments; C075222:amyloid beta-protein (1-42)