Cholecystokinin depolarizes guinea pig sphincter of Oddi neurons by activating CCK-A receptors.
Cholecystokinin depolarizes guinea pig sphincter of Oddi neurons by activating CCK-A receptors.
复制标题
DOI：
10.1152/ajpgi.1997.272.6.g1365
复制
发表时间：
1997-06
期刊：
影响因子：
--
通讯作者：
Alexander P. Gokin;Kirk Hillsley;G. Mawe
中科院分区：
文献类型：
--
作者：
Alexander P. Gokin;Kirk Hillsley;G. Mawe
运动研究表明，胆囊收缩素（CCK）在饭后通过Oddi括约肌（SO）的神经机制起作用。为了评估其在SO神经节中的作用，CCK通过微射（0.1 mM）或灌注（0.1 ~ 300 nM）的方式施加，同时在完整的SO神经元细胞内进行记录。在强直性细胞中，CCK的微抛射和灌注引起长时间的去极化，并伴有动作电位。在相细胞中，CCK微抛射引起短暂和/或延长的去极化，而超融合只引起延长的去极化。在超极化后的细胞中，CCK未引起静息膜电位的可检测变化。在低na + Krebs溶液中，强直细胞和相细胞的长时间去极化均明显减少。无硫CCK （100 nM）无影响。CCK-A受体拮抗剂能显著降低cck诱导的去极化，而CCK-B受体拮抗剂则不能。由此可见，CCK可作用于CCK- a受体使SO神经元去极化。然而，激素CCK不太可能介导这种作用，因为SO神经元对CCK的敏感性与饭后血清中CCK的峰值浓度之间存在差异。
Motility studies indicate that cholecystokinin (CCK) acts through a neural mechanism in the sphincter of Oddi (SO) after meals. To evaluate its actions in SO ganglia, CCK was applied by microejection (0.1 mM) or superfusion (0.1 to 300 nM) while recording was carried out intracellularly from intact SO neurons. In tonic cells, microejection and superfusion of CCK caused a prolonged depolarization accompanied by action potentials. In phasic cells, microejection of CCK caused brief and/or prolonged depolarizations, but superfusion caused only prolonged depolarizations. In afterhyperpolarized cells, CCK did not cause a detectable change in the resting membrane potential. In low-Na+ Krebs solution, the prolonged depolarizations in both tonic and phasic cells were significantly reduced. Unsulfated CCK (100 nM) had no effect. CCK-induced depolarization was significantly reduced by a CCK-A, but not a CCK-B, receptor antagonist. It is concluded that CCK can act on CCK-A receptors to depolarize SO neurons. However, it is unlikely that hormonal CCK could mediate such an action because of the discrepancy between the sensitivity of SO neurons for CCK and the peak concentrations of CCK in the serum after a meal.