Hirota K, Lambert D G
University Department of Anaesthesia, Leicester Royal Infirmary, UK.
Neurosci Lett. 1997 Feb 28;223(3):169-72. doi: 10.1016/s0304-3940(97)13434-6.
Radioligand binding studies using the L-type voltage sensitive Ca2+ channel (VSCC) antagonist (+)-[3H]PN200-110 revealed the following rank order channel density in rat brain and cultured neuronal cell homogenates: striatum > or = cerebrocortex > > cerebellum = brainstem > SH-SY5Y cell line > NG108-15 cell line > 1321N1 cell line > PC12 cell line. There were no significant differences in the equilibrium dissociation constant, Kd for (+)-[3H]PN200-110 or pK50 for nifedipine. K+ depolarization in SH-SY5Y cells and NG108-15 cells evoked a biphasic and monophasic increase in [Ca2+]i. The L-type Ca2+ channel antagonist nifedipine (1 microM) produced a 66 and 87% inhibition of the K(+)-evoked rise in the peak and plateau phase [Ca2+]i in SH-SY5Y cells and abolished the monophasic response in NG108-15 cells. The L-channel activator S(-)Bay K 8644 (1 microM) enhanced the K(+)-evoked increase in [Ca2+]i in both cell lines. These data demonstrate a comparatively low density of L-VSCC in undifferentiated SH-SY5Y cells, NG108-15 cells, 1321N1 cells and PC12 cells that are functionally active in at least SH-SY5Y cells and NG108-15 cells.
使用 L 型电压敏感钙通道（VSCC）拮抗剂（+）-[³H]PN200-110 的放射性配体结合研究揭示了大鼠脑和培养神经元细胞匀浆中通道密度的以下排序：纹状体≥大脑皮质＞＞小脑 = 脑干＞SH-SY5Y 细胞系＞NG108-15 细胞系＞1321N1 细胞系＞PC12 细胞系。（+）-[³H]PN200-110 的平衡解离常数 Kd 或硝苯地平的 pK50 没有显著差异。SH-SY5Y 细胞和 NG108-15 细胞中的 K⁺去极化引起细胞内钙离子浓度（[Ca²⁺]i）双相和单相增加。L 型钙通道拮抗剂硝苯地平（1μM）对 SH-SY5Y 细胞中 K⁺诱发的[Ca²⁺]i 峰值和平台期升高产生 66%和 87%的抑制，并消除了 NG108-15 细胞中的单相反应。L 通道激活剂 S（-）Bay K 8644（1μM）增强了两种细胞系中 K⁺诱发的[Ca²⁺]i 增加。这些数据表明，在未分化的 SH-SY5Y 细胞、NG108-15 细胞、1321N1 细胞和 PC12 细胞中，L-VSCC 的密度相对较低，其中至少 SH-SY5Y 细胞和 NG108-15 细胞具有功能活性。
