Kammermeier P J, Ikeda S R
Laboratory of Molecular Physiology, Guthrie Research Institute, Sayre, Pennsylvania 18840, USA.
Neuron. 1999 Apr;22(4):819-29. doi: 10.1016/s0896-6273(00)80740-0.
Group I mGluRs heterologously expressed in sympathetic neurons inhibited calcium (I(Ca)) and M-type potassium (I(M)) currents. Treatment with pertussis toxin (PTX) revealed a voltage-dependent (VD), PTX-sensitive component of I(Ca) inhibition and a voltage-independent (VI), PTX-insensitive component. Coexpression of RGS2 occluded mGluR1a inhibition of I(M) and made I(Ca) inhibition VD in PTX-treated cells, presumably by blocking the effects of G alpha(q/11)-GTP. These data indicate that mGluR1a can couple to G(i/o) as well as G(q/11). In addition, VI I(Ca) inhibition proceeds through a G alpha(q/11)-GTP-mediated pathway, which can be occluded by expressing RGS2, leaving the VD, G betagamma-mediated inhibition active. These data may reveal a functional role for the upregulation of RGS2 expression in in vivo systems.
在交感神经元中异源表达的I组代谢型谷氨酸受体（mGluRs）抑制钙电流（I(Ca)）和M型钾电流（I(M)）。百日咳毒素（PTX）处理显示I(Ca)抑制存在电压依赖性（VD）、对PTX敏感的成分以及电压非依赖性（VI）、对PTX不敏感的成分。RGS2的共表达消除了mGluR1a对I(M)的抑制作用，并使PTX处理细胞中的I(Ca)抑制呈电压依赖性，这可能是通过阻断Gα(q/11)-GTP的作用实现的。这些数据表明mGluR1a可以与G(i/o)以及G(q/11)偶联。此外，VI I(Ca)抑制通过Gα(q/11)-GTP介导的途径进行，该途径可通过表达RGS2而被阻断，使VD、Gβγ介导的抑制作用保持活性。这些数据可能揭示了RGS2表达上调在体内系统中的功能作用。
