Key Concepts of Section 15.4

• The cardiac muscarinic acetylcholine receptor is a GPCR whose effector protein is a K⁺ channel. Receptor activation releases the G_βγ subunit, which binds to and opens K⁺ channels (see Figure 15-17). The resulting hyperpolarization of the cell membrane slows the rate of heart muscle contraction.

• Rhodopsin, the photosensitive GPCR in rod cells, comprises the protein opsin linked to 11-cis-retinal. Light-induced isomerization of the 11-cis-retinal moiety produces activated opsin, which then activates the coupled heterotrimeric G protein transducin (G_t) by catalyzing exchange of free GTP for bound GDP on the G_αt subunit (see Figures 15-19 and 15-20).

• The effector protein in the rhodopsin pathway is PDE, which is activated by the G_αt·GTP-mediated release of inhibitory subunits. Reduction in the cGMP level by this enzyme leads to closing of cGMP-gated Na⁺/Ca²⁺ channels, hyperpolarization of the membrane, and decreased release of neurotransmitter (see Figure 15-20).

• Several mechanisms act to terminate visual signaling: GAP proteins inactivate G_αt·GTP, Ca²⁺-sensing proteins activate guanylate cyclase, and rhodopsin phosphorylation and binding of arrestin inhibit activation of transducin.

• Adaptation to a wide range of ambient light levels is mediated by movements of transducin and arrestin into and out of the rod-cell outer segment, which together modulate the ability of small increases in light levels to activate the downstream effector PDE, and thus the sensitivity of the rod cell in different ambient levels of light.