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乙醇对培养颈上神经节神经元烟碱型乙酰胆碱受体的影响 被引量:1

Ethanol Inhibits Nicotinc Acetylcholine Receptors in Cultured Superior Cervical Ganglion Neurons
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摘要 目的:探讨乙醇对培养颈上神经节神经元烟碱型乙酰胆碱受体(nAChRs)的影响。方法:培养新生12h的Wistar大鼠颈上神经节神经元,全细胞膜片钳法记录烟碱诱发电流,观察乙醇对烟碱诱发电流的作用及是否存在浓度依赖性、电压依赖性、使用依赖性,并观察乙醇对颈上神经节神经元nAChRs脱敏的影响。结果:在钳制电位-70mV,乙醇浓度依赖性抑制烟碱诱发电流,IC50(半量抑制率)为(45.55±3.62)mmol/L,可加速nAChRs脱敏,但乙醇对烟碱诱发电流的抑制作用无使用依赖性及电压依赖性。结论:乙醇显著抑制培养的颈上神经节神经元烟碱型nAChRs,其作用位点可能是nAChRs细胞膜外的变构性调节位点。 Objective. To determine the effects of ethanol on nicotinic acetylcholine recep- tors (nAChRs) in cultured primary superior cervical ganglion neurons. Methods: The acute effects of ethanol on nAChRs in cultured primary superior cervical ganglion neurons (SCGs) were examined by whole-cell patch clamp recordings. After the whole-cell configuration formed, drugs diluted to the desired concentrations before using, were applied directly to the single neurons. Results: Holding at --70 mV, inhibition rate of higher concentration of ethanol was larger than that of the lower one. The ICs0 was (45.55+3.62) mmol/L. Ethanol (50 mmol/L) accelerated the slow decay but did not accelerate the quick decay of nicotine-evoked current (INic) in $CGs. There was no use-dependence and voltage-dependence of ethanol on suppressing INic in SCGs. Conclusion: Ethanol significantly inhibits the whole cell INic in SCGs, probably in a noncompeti- tive inhibition manner in extra-membrane sites.
出处 《神经损伤与功能重建》 2011年第6期391-395,共5页 Neural Injury and Functional Reconstruction
基金 国家自然科学基金(No.30900459) 国家教育部新教师基金(No.090392) 湖北省教育厅科学技术研究计划指导性项目(B) 武汉大学青年教师资助项目(No.3082012)
关键词 乙醇 颈上神经节 烟碱 脱敏 ethanol superior cervical ganglion nicotine desensitization
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  • 1汪海,崔文玉,刘传缋.烟碱对大脑皮层毒蕈碱型受体与其激动剂和拮抗剂结合的调节[J].中国药理学报,1996,17(6):497-499. 被引量:1
  • 2刘传缋 周宏灏.抗胆碱药在神经元N受体上作用位点的分析.分子药理学[M].哈尔滨:黑龙江科学技术出版社,1999.116-127.
  • 3Kilpatrick DL, Slepetis RJ, Corcoran JJ, et al. Calcium uptake and catecholamine secretion by cultured bovine adrenal medulla cells [J]. J Neurochem, 1982, 38(2): 427-435.
  • 4Wada A, Takara H, Izumi F, et al. Influx of Na+ through acetylcholine receptor- associated Na + channels: relationship between 22 Na + influx, 45 Ca2 + and secretion of catecholamines in cultured bovine adrenal medulla cell[J]. Neuroscience, 1985, 15(1):
  • 5Liu JH, Jorgensen MS, Adams JM, et al. Ceramide modulate nicotine receptor- dependent Ca2 + signaling in rat chromaffin cells[J]. J Neurosci, 2001, 66(4): 559-564.
  • 6JorgensenMS, Liu JH, Adams JM, etal. Inhibition of voltage -gated Ca2+ current by PACAP in rat adredal chromaffin cells[J]. Regul Pept, 2002, 103(1): 59-65.
  • 7Roberts DL, Arneric SP, Sullivan JP. Functional modulation of human ''ganglionic- like'' neuronal nicotine acetylcholine receptor (nAChRs) by L - type calcium channel antagonists[J]. Biochem Biophys Res Commun, 1995, 213(2): 657-662.
  • 8Fernandez JM, Granja R, Izaguirre V, et al. ω- conotoxin GVIA blocks nicotine - induced catecholamine secretion by blocking the nicotine receptor - activated inward currents in bovine chromaffin cells [ J ]. Neurosci Lett, 1995, 191 ( 1 -2): 59-62.
  • 9Rowell P P, Li M. Dose-response relationship for nicotine-induced up-regulation of rat brain nicotinic receptors [J]. Neurochem, 1997, 68:1982-1989.
  • 10Barrantes G E, Murphy C T, Westwick J, et al. Nicotine increases intracellular calcium in rat hippocampal neurons via voltage-gated calcium channels[J]. Neurosci Lett, 1995, 196:101-104.

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