Murphy N P, Ball S G, Vaughan P F
Department of Cardiovascular Studies, University of Leeds, England.
J Neurochem. 1991 May;56(5):1810-5. doi: 10.1111/j.1471-4159.1991.tb02085.x.
The human neuroblastoma clone SH-SY5Y expresses potassium-, carbachol-, and calcium ionophore A23187-evoked, calcium-dependent release of [3H]noradrenaline. Release in response to carbachol and potassium was greater than additive. Atropine (Ki = 0.33 nM), hexahydrosiladifenidol (Ki = 18 nM), and pirenzepine (Ki = 1,183 nM) completely inhibited the carbachol-evoked noradrenaline release, an order of potency suggesting that an M3 receptor was linked to release. In contrast, noradrenaline release was only partially inhibited by the M2-selective antagonists methoctramine (10(-4) M) and AFDX-116 (10(-4) M), by approximately 14 and 46%, respectively. The nicotinic antagonist d-tubocurarine (10(-4) M) resulted in a partial inhibition of release, a finding suggesting that a nicotinic receptor may also be involved. SH-SY5Y provides a suitable cell line in which to study the biochemical mechanisms underlying the cholinergic receptor regulation of noradrenaline release.
人神经母细胞瘤克隆株SH - SY5Y表现出钾离子、卡巴胆碱和钙离子载体A23187诱发的、钙依赖性的[3H]去甲肾上腺素释放。对卡巴胆碱和钾离子的释放反应大于两者单独作用之和。阿托品(Ki = 0.33 nM)、六氢硅双苯啶(Ki = 18 nM)和哌仑西平(Ki = 1183 nM)完全抑制了卡巴胆碱诱发的去甲肾上腺素释放,这种效价顺序表明M3受体与释放相关。相比之下,M2选择性拮抗剂甲溴东莨菪碱(10^(-4) M)和AFDX - 116(10^(-4) M)仅部分抑制去甲肾上腺素释放,分别约为14%和46%。烟碱拮抗剂筒箭毒碱(10^(-4) M)导致释放部分受抑制,这一发现表明烟碱受体可能也参与其中。SH - SY5Y提供了一个合适的细胞系,可用于研究胆碱能受体调节去甲肾上腺素释放的生化机制。