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 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.
Kammermeier
P J
PJ
Laboratory of Molecular Physiology, Guthrie Research Institute, Sayre, Pennsylvania 18840, USA.
Ikeda
S R
SR
D000818:Animals; D015220:Calcium Channels / Q000378:metabolism*; D019204:GTP-Binding Proteins / Q000378:metabolism*; D066298:In Vitro Techniques; D009474:Neurons / Q000378:metabolism; D018408:Patch-Clamp Techniques; D037342:Pertussis Toxin; D015221:Potassium Channels / Q000378:metabolism*; D051381:Rats; D018094:Receptors, Metabotropic Glutamate / Q000378:metabolism*; D011993:Recombinant Fusion Proteins / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology*; D013564:Sympathetic Nervous System / Q000378:metabolism; D010566:Virulence Factors, Bordetella / Q000494:pharmacology
D015220:Calcium Channels; D015221:Potassium Channels; D018094:Receptors, Metabotropic Glutamate; D011993:Recombinant Fusion Proteins; D010566:Virulence Factors, Bordetella; D037342:Pertussis Toxin; D019204:GTP-Binding Proteins