Oxford G S, Tse A
Department of Physiology, University of North Carolina, Chapel Hill 27599.
Biol Reprod. 1993 Jan;48(1):1-7. doi: 10.1095/biolreprod48.1.1.
The role of ion channel activity in the response of rat pituitary lactotrophs and gonadotrophs to dopamine (DA) and GnRH, respectively, was investigated. Single lactotrophs and gonadotrophs were unambiguously identified with the reverse hemolytic plaque assay, and recordings of membrane potential and current were obtained using whole-cell and single-channel patch-clamp techniques. In lactotrophs, DA inhibited spontaneous electrical activity by activating a K+ conductance that hyperpolarized the cells. A 50 pS K+ channel underlies this response and was activated following agonist binding to a D2 type receptor via a "direct" interaction with a pertussis toxin-sensitive G-protein. In gonadotrophs, GnRH triggers rhythmic hyperpolarizations due also to a K+ conductance increase. The K+ channel underlying the GnRH response is an apamin-sensitive, Ca(2+)-activated channel. Although both agonists produce hyperpolarizations in their respective target cells via K+ channel activation, differences in intracellular calcium response probably discriminate the stimulatory (GnRH) and inhibitory (DA) actions on hormone secretion. Each K+ channel type plays a different role in modulating the intracellular Ca2+ levels to yield these actions.
分别研究了离子通道活性在大鼠垂体催乳素细胞和促性腺激素细胞对多巴胺（DA）和促性腺激素释放激素（GnRH）反应中的作用。采用反向溶血空斑试验明确鉴定单个催乳素细胞和促性腺激素细胞，并使用全细胞和单通道膜片钳技术记录膜电位和电流。在催乳素细胞中，DA通过激活使细胞超极化的K⁺电导来抑制自发电活动。一种50 pS的K⁺通道是这种反应的基础，并且在激动剂通过与百日咳毒素敏感的G蛋白“直接”相互作用结合到D2型受体后被激活。在促性腺激素细胞中，GnRH也由于K⁺电导增加而引发节律性超极化。GnRH反应所涉及的K⁺通道是一种蜂毒明肽敏感的、Ca²⁺激活的通道。尽管两种激动剂都通过激活K⁺通道在各自的靶细胞中产生超极化，但细胞内钙反应的差异可能区分了对激素分泌的刺激作用（GnRH）和抑制作用（DA）。每种K⁺通道类型在调节细胞内Ca²⁺水平以产生这些作用方面发挥着不同的作用。
