Court J A, Fowler C J, Candy J M, Hoban P R, Smith C J
Naunyn Schmiedebergs Arch Pharmacol. 1986 Sep;334(1):10-6. doi: 10.1007/BF00498734.
The influence of the ambient potassium ion concentration ([K+]) upon agonist stimulated hydrolysis of phosphoinositides (PI) has been studied in isolated miniprisms of rat hippocampus and cerebral cortex. When the external [K+] was raised from 6 to 18 mmol/l, there was little or no increase in the hydrolysis of PI in the absence of agonist, however, carbachol (100 mumol/l) stimulated hydrolysis was greatly enhanced in both brain regions studied. Thus, carbachol stimulated the hydrolysis of PI to 146% and 386% of control levels at potassium concentrations of 5.88 and 18.2 mmol/l, respectively, in the rat hippocampus. A similar enhancement of muscarine (100 mumol/l) stimulation was observed in cortical miniprisms with 18 mmol/l [K+]. A further enhancement was seen at higher ambient [K+], although basal hydrolysis of PI was then also increased. The carbachol-stimulated hydrolysis of PI found at both 6 and raised [K+] was prevented by atropine (1 and 10 mumol/l) and tetraethylammonium (20 mmol/l), but not by 10 mmol/l Mg2+. Pirenzepine (50 nmol/l) also reduced this response. The ions Cs+ and Rb+ (but not Li+ or Tris+) produced a similar enhancement of the carbachol stimulation to that found with K+. At a buffer [K+] of 6 mmol/l, noradrenaline (100 mumol/l) produced a 2-fold increase in the hydrolysis of PI whereas 5-hydroxytryptamine (100 mumol/l) and histamine (500 mumol/l) had little or no effect. However, histamine and 5-hydroxytryptamine did stimulate the hydrolysis of PI when [K+] was increased. Miniprism ATP content was not changed by a rise in [K+] to 18 mmol/l. The significance of these results is discussed in terms of the postsynaptic cellular events following cholinergic stimulation.
已在大鼠海马体和大脑皮层的离体微小切片中研究了细胞外钾离子浓度（[K⁺]）对激动剂刺激的磷酸肌醇（PI）水解的影响。当细胞外[K⁺]从6 mmol/L升高到18 mmol/L时，在无激动剂的情况下，PI水解几乎没有增加或没有增加，然而，在所研究的两个脑区中，卡巴胆碱（100 μmol/L）刺激的水解均显著增强。因此，在大鼠海马体中，钾离子浓度分别为5.88和18.2 mmol/L时，卡巴胆碱刺激的PI水解分别达到对照水平的146%和386%。在[K⁺]为18 mmol/L的皮层微小切片中观察到毒蕈碱（100 μmol/L）刺激有类似增强。在更高的细胞外[K⁺]时观察到进一步增强，尽管此时PI的基础水解也增加了。在6 mmol/L和升高的[K⁺]时发现的卡巴胆碱刺激的PI水解被阿托品（1和10 μmol/L）和四乙铵（20 mmol/L）抑制，但不被10 mmol/L Mg²⁺抑制。哌仑西平（50 nmol/L）也降低了这种反应。离子Cs⁺和Rb⁺（但不是Li⁺或Tris⁺）对卡巴胆碱刺激的增强作用与K⁺相似。在缓冲液[K⁺]为6 mmol/L时，去甲肾上腺素（100 μmol/L）使PI水解增加了2倍，而5-羟色胺（100 μmol/L）和组胺（500 μmol/L）几乎没有影响或没有影响。然而，当[K⁺]增加时，组胺和5-羟色胺确实刺激了PI的水解。将[K⁺]升高到18 mmol/L不会改变微小切片中的ATP含量。根据胆碱能刺激后的突触后细胞事件讨论了这些结果的意义。
