Login I S, Kuan S I, Judd A M, MacLeod R M
Department of Neurology, University of Virginia School of Medicine, Charlottesville.
Cell Calcium. 1990 Sep;11(8):525-30. doi: 10.1016/0143-4160(90)90028-s.
The MMQ pituitary cell line, which expresses a membranal dopamine receptor, was used to examine the individual contributions of dopamine and protein kinase C (PKC) to control of the intracellular calcium concentration. The calcium concentrations, monitored with the fluorescent dye Indo-1, increased in response to elevated K+, BAY K8644, and maitotoxin, implicating the presence of voltage-dependent calcium channels. Dopamine had no detectable independent effect, but significantly inhibited the rise in intracellular calcium mediated by activation of voltage-dependent calcium channels; this dopaminergic action was prevented by haloperidol. Acute pharmacological activation of PKC for 60 s inhibited the stimulatory effects of these calcium channel activators, and this acute inhibitory action was abolished by prior depletion of PKC. In contrast, however, PKC depletion did not alter the calcium response to BAY K8644 or maitotoxin. Thus, MMQ cells appear to have voltage-dependent calcium channels which, at rest, are either at low density or in a closed state. The rise in intracellular calcium resulting from stimulation of the channels is under inhibitory control by an apparent D-2 dopamine receptor. When pharmacologically activated, phorbol diester-sensitive PKC limits the rise in the cellular calcium level associated with calcium uptake. In the absence of pharmacological activation, however, this enzyme system does not appear to play a role in the cellular calcium response to BAY K8644 or maitotoxin.
表达膜性多巴胺受体的MMQ垂体细胞系用于研究多巴胺和蛋白激酶C（PKC）对细胞内钙浓度控制的单独作用。用荧光染料Indo-1监测的钙浓度，在高钾、BAY K8644和 maitotoxin作用下升高，提示存在电压依赖性钙通道。多巴胺无明显独立作用，但能显著抑制电压依赖性钙通道激活介导的细胞内钙升高；这种多巴胺能作用可被氟哌啶醇阻断。PKC的急性药理学激活60秒可抑制这些钙通道激活剂的刺激作用，且这种急性抑制作用可被预先耗尽PKC所消除。然而，相比之下，PKC耗尽并未改变对BAY K8644或maitotoxin的钙反应。因此，MMQ细胞似乎具有电压依赖性钙通道，在静息状态下，这些通道要么密度低，要么处于关闭状态。通道刺激引起的细胞内钙升高受一种明显的D-2多巴胺受体的抑制性控制。当药理学激活时，佛波酯敏感的PKC限制与钙摄取相关的细胞钙水平升高。然而，在没有药理学激活的情况下，该酶系统似乎在细胞对BAY K8644或maitotoxin的钙反应中不起作用。
