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钾离子对大鼠脑突触神经小体中兴奋性氨基酸和卡巴胆碱引发的肌醇磷酸形成有不同影响。

K+ differentially affects the excitatory amino acids- and carbachol-elicited inositol phosphate formation in rat brain synaptoneurosomes.

作者信息

Guiramand J, Nourigat A, Sassetti I, Recasens M

机构信息

Centre CNRS-INSERM de Pharmacologie-Endrocrinologie, Montpellier, France.

出版信息

Neurosci Lett. 1989 Mar 27;98(2):222-8. doi: 10.1016/0304-3940(89)90514-4.

DOI:10.1016/0304-3940(89)90514-4
PMID:2565568
Abstract

K+, excitatory amino acids (EAAs) and carbachol (Carb) were tested separately or in pairs for their ability to stimulate inositol phosphate (IPs) formation in rat forebrain synaptoneurosomes. K+ ions per se, stimulate IPs synthesis (158% of the control value) as well as EAAs and Carb. The glutamate (Glu)- and quisqualate (QA)-elicited IPs formation is not additive with that evoked by K+. Inversely, K+ ions (up to 30 mM) potentiate the Carb-induced IPs accumulation. These results indicate that QA (or Glu) and Carb enhance IPs formation independently and that QA- and K+ -induced IPs responses are interdependent. This suggests that they share a 'common intermediate' step in the multistep mechanism which leads from receptor activation to the IPs synthesis. This 'common intermediate' step may be depolarization and/or Na+ influx.

摘要

分别或成对测试钾离子(K⁺)、兴奋性氨基酸(EAAs)和卡巴胆碱(Carb)刺激大鼠前脑突触神经小体中肌醇磷酸(IPs)形成的能力。钾离子本身可刺激IPs合成(为对照值的158%),EAAs和Carb也有此作用。谷氨酸(Glu)和quisqualate(QA)引发的IPs形成与钾离子引发的并非相加关系。相反,钾离子(高达30 mM)可增强Carb诱导的IPs积累。这些结果表明,QA(或Glu)和Carb独立增强IPs形成,且QA和钾离子诱导的IPs反应相互依赖。这表明它们在从受体激活到IPs合成的多步骤机制中共享一个“共同中间”步骤。这个“共同中间”步骤可能是去极化和/或钠离子内流。

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