Tiger G, Björklund P E, Fowler C J
Department of Pharmacology, University of Umeå, Sweden.
Neurosci Lett. 1990 Jul 31;115(2-3):243-7. doi: 10.1016/0304-3940(90)90462-i.
Raising the assay [K+] from 6 to 18 mM enhances the inositol phospholipid breakdown response to carbachol in rat brain miniprisms. In the frontal cortex, the degree of enhancement by K+ was independent of the carbachol concentration used, whereas in the striatum, a significantly higher degree of enhancement was seen at 1000 than at 50 microM carbachol. The carbachol-stimulated inositol phospholipid breakdown was antagonized by pirenzepine at both [K+] with potencies suggesting involvement of M1-type muscarinic receptors in the frontal cortex and both M1- and M2-type muscarinic receptors in the striatum. It is suggested that the response mediated by the M1-type receptors is enhanced to a greater degree by raised [K+] than that mediated by the M2-type receptors.
将测定的[K⁺]浓度从6 mM提高到18 mM可增强大鼠脑薄片中对卡巴胆碱的肌醇磷脂分解反应。在额叶皮质中，K⁺的增强程度与所用卡巴胆碱的浓度无关，而在纹状体中，在1000 μM卡巴胆碱时比在50 μM卡巴胆碱时观察到显著更高的增强程度。在两种[K⁺]浓度下，哌仑西平均可拮抗卡巴胆碱刺激的肌醇磷脂分解，其效力表明额叶皮质中M1型毒蕈碱受体参与其中，而纹状体中M1型和M2型毒蕈碱受体均参与其中。提示M1型受体介导的反应比M2型受体介导的反应在升高的[K⁺]浓度下增强程度更大。
