钾对大鼠大脑皮质微小切片中卡巴胆碱刺激的肌醇磷脂分解的增强作用：与其他去极化剂的比较。

Enhancement by potassium of carbachol-stimulated inositol phospholipid breakdown in rat cerebral cortical miniprisms: comparison with other depolarising agents.

作者信息

Tiger G, Björklund P E, Cowburn R F, Fowler C J

机构信息

Department of Pharmacology, University of Umeå, Sweden.

出版信息

J Neurochem. 1989 Jun;52(6):1843-53. doi: 10.1111/j.1471-4159.1989.tb07266.x.

DOI:10.1111/j.1471-4159.1989.tb07266.x

PMID:2470855

Abstract

Increasing the [K+] in the assay medium from 5.7 to 17.8 mM produces a large enhancement of the inositol phospholipid breakdown response to the muscarinic agonist carbachol in rat cerebral cortical miniprisms, with minor effects on basal inositol phospholipid breakdown. This effect is also found with Rb+. The enhancement by a raised [K+] is not accompanied by a change in the composition of the labelled polyphosphoinositides. The carbachol-stimulated inositol phospholipid breakdown at 17.8 and 42.7 mM K+ was antagonised by veratrine (5-80 microM), 4-aminopyridine (5 mM), and tetraethylammonium (20 mM). These compounds, however, also inhibited the binding of [3H]quinuclidinyl benzilate to cortical membranes. BRL 34915 (0.2-20 microM) was without significant effect on carbachol-stimulated inositol phospholipid breakdown at either 5.7 or 17.8 mM K+.Mg2+ (10 mM) considerably reduced the carbachol-stimulated inositol phospholipid breakdown at 17.8, but not 42.7, mM K+. Inositol phospholipid breakdown was also stimulated, albeit to a small extent, by L-glutamate (100-3,000 microM) and quisqualate (1-100 microM), with the stimulation being additive to that produced by carbachol at both 5.7 and 17.8 mM K+. N-Methyl-D-aspartate (10-1,000 microM in Mg2+-free medium) had no significant effect on basal inositol phospholipid breakdown and had little or no effect on carbachol-stimulated inositol phospholipid breakdown at either 5.7 or 17.8 mM K+. It is concluded that it may not be correct to ascribe wholly the enhancement by K+ of carbachol-stimulated inositol phospholipid breakdown to the tissue-depolarising actions of this ion and that other actions of K+ may be involved.

摘要

将测定介质中的[K⁺]浓度从5.7 mM提高到17.8 mM，可使大鼠大脑皮层小块组织对毒蕈碱激动剂卡巴胆碱的肌醇磷脂分解反应大幅增强，而对基础肌醇磷脂分解的影响较小。用Rb⁺时也发现了这种效应。升高的[K⁺]所产生的增强作用并不伴随着标记的多磷酸肌醇组成的变化。在17.8 mM和42.7 mM K⁺浓度下，卡巴胆碱刺激的肌醇磷脂分解受到藜芦碱（5 - 80 μM）、4 - 氨基吡啶（5 mM）和四乙铵（20 mM）的拮抗。然而，这些化合物也抑制了[³H]喹核醇基苯甲酸酯与皮层膜的结合。BRL 34915（0.2 - 20 μM）在5.7 mM或17.8 mM K⁺浓度下对卡巴胆碱刺激的肌醇磷脂分解均无显著影响。Mg²⁺（10 mM）在17.8 mM K⁺浓度下可显著降低卡巴胆碱刺激的肌醇磷脂分解，但在42.7 mM K⁺浓度下则无此作用。L - 谷氨酸（100 - 3000 μM）和quisqualate（1 - 100 μM）也能刺激肌醇磷脂分解，尽管程度较小，且在5.7 mM和1 mM K⁺浓度下，它们与卡巴胆碱产生的刺激作用具有相加性。在无Mg²⁺的介质中，N - 甲基 - D - 天冬氨酸（10 - 1000 μM）对基础肌醇磷脂分解无显著影响，在5.7 mM或17.8 mM K⁺浓度下对卡巴胆碱刺激的肌醇磷脂分解也几乎没有影响。得出的结论是，将K⁺对卡巴胆碱刺激的肌醇磷脂分解的增强作用完全归因于该离子的组织去极化作用可能并不正确，K⁺的其他作用可能也参与其中。