Pitler T A, McCarren M, Alger B E
Department of Physiology, University of Maryland School of Medicine, Baltimore 21201.
Neurosci Lett. 1988 Aug 31;91(2):177-82. doi: 10.1016/0304-3940(88)90764-1.
Using intracellular recording techniques in the rat hippocampal slice, we observed that muscarinic agonists produce a transient Ca2+-dependent depolarization that may be related to the phosphatidylinositol cycle. First, it was more readily produced by muscarinic group A agonists, which strongly enhance the breakdown of phosphatidylinositol-4,5-bisphosphate (PIP2) than by group B agonists, which are less efficacious. Second, the Ca2+-dependent response was blocked by pirenzepine (PRZ), a selective muscarinic antagonist that blocks PIP2 breakdown in forebrain. Both group A and group B muscarinic agonists caused equivalent maintained levels of depolarization that were relatively insensitive to PRZ. The data suggest that the Ca2+-dependent response is fundamentally unlike other muscarinic responses that have been described in hippocampus.
运用大鼠海马脑片的细胞内记录技术,我们观察到毒蕈碱激动剂会产生一种短暂的钙依赖性去极化,这可能与磷脂酰肌醇循环有关。首先,毒蕈碱A组激动剂比B组激动剂更易产生这种去极化,前者能强烈增强磷脂酰肌醇 - 4,5 - 二磷酸(PIP2)的分解,而后者的效力较低。其次,钙依赖性反应被哌仑西平(PRZ)阻断,PRZ是一种选择性毒蕈碱拮抗剂,可阻断前脑PIP2的分解。A组和B组毒蕈碱激动剂都引起了相当的去极化维持水平,且对PRZ相对不敏感。这些数据表明,钙依赖性反应与海马体中描述的其他毒蕈碱反应根本不同。