Suzuki N, Kudo Y, Takagi H, Yoshioka T, Tanakadate A, Kano M
Department of Physiology, School of Medicine, Kitasato University, Kanagawa, Japan.
J Cell Physiol. 1990 Jul;144(1):62-8. doi: 10.1002/jcp.1041440109.
Participation of two types of Ca2+ channels (T- and L-types) in the sustained increase of cytosolic-free Ca2+ concentration [( Ca2+]i) was studied in thyrotropin-releasing hormone (TRH)-stimulated clonal GH3 pituitary cells. The effects of Ca2+ channel blockers were analyzed by measuring Ca2+ channel current and [Ca2+]i, using whole-cell voltage-clamp and Fura-2 fluorometry, respectively. Phenytoin (100 microM) and Ni2+ (100 microM) selectively blocked T-type Ca2+ channels and suppressed the TRH-induced sustained [Ca2+]i increase in single cells. Synthetic omega-conotoxin (omega-CgTX, 2 microM) preferentially blocked L-type Ca2+ channels, but it did not suppress the TRH-induced sustained [Ca2+]i increase. The present results suggest that the sustained elevations of [Ca2+]i triggered by TRH may be mediated by T-type Ca2+ channels in GH3 cells.
在促甲状腺激素释放激素（TRH）刺激的克隆GH3垂体细胞中，研究了两种类型的Ca2+通道（T型和L型）参与胞质游离Ca2+浓度（[Ca2+]i）持续升高的情况。分别使用全细胞膜片钳和Fura-2荧光测定法，通过测量Ca2+通道电流和[Ca2+]i来分析Ca2+通道阻滞剂的作用。苯妥英（100微摩尔）和Ni2+（100微摩尔）选择性阻断T型Ca2+通道，并抑制TRH诱导的单细胞中[Ca2+]i的持续升高。合成的ω-芋螺毒素（ω-CgTX，2微摩尔）优先阻断L型Ca2+通道，但它不抑制TRH诱导的[Ca2+]i持续升高。目前的结果表明，TRH触发的[Ca2+]i持续升高可能由GH3细胞中的T型Ca2+通道介导。
