Expression of RGS2 alters the coupling of metabotropic glutamate receptor 1a to M-type K+ and N-type Ca2+ channels

Group I mGluRs heterologously expressed in sympathetic neurons inhibited ca lcium (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. C oexpression of RGS2 occluded mGluR1a inhibition of I-M and made I-Ca inhibi tion 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 a s 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 th e VD, G beta gamma-mediated inhibition active. These data may reveal a func tional role for the upregulation of RGS2 expression in in vivo systems.