Figure 1. Schematic representation of intracellular events leading to homologous and heterologous desensitization following activation of -adrenergic receptor (-AR). -AR couples to G_s leading to activation of AC. Agonist activated -AR is phosphorylated by -ARK at its C-terminus. Phosphorylated -AR interacts with -arrestin that prevents G_s activation by the receptor (homologous desensitization). -arrestin also acts as an adaptor protein to facilitate -AR internalization and to engage -AR to MAP kinase (MAPK) pathway. In heterologous desensitization, -AR is phosphorylated by protein kinases other than -ARK. For example PKA, which is activated by cAMP can modify -AR leading to diminished receptor activity towards G_s. Phosphorylated serine/threonine residues in -AR are labelled as orange dots.

Figure 2. Rhodopsin mediates visual transduction in the rod outer segments (ROS). ROS are specialized compartments consisting of 2000 discs which are invaginated plasma membranes (lower panel). Shown in the upper panel is a section of ROS depicting signalling proteins and their distribution in disc or plasma membranes. Light activates rhodopsin by triggering isomerization of 11-cis retinal to become all-trans retinal in rhodopsin. Activated rhodopsin interacts with transducin (Gt), which turns on a cGMP phosphodiesterase (PDE). PDE catalyses the hydrolysis of cGMP leading to a reduced level of cGMP. Cyclic GMP is generated by guanylate cyclase (GC) and is responsible for opening of cGMP channels in the plasma membrane. Light leads to hyperpolarization of photoreceptors due to breakdown of cGMP resulting in closure of cGMP channels.To terminate the activity of activated rhodopsins, rhodopsin kinase modifies rhodopsins by phosphorylation. Phosphorylated rhodopsin interacts with arrestin that prevents its activity to activate Gt. Stable rhodopsin/arrestin complexes may be internalized for degradation of rhodopsins and to initiate apoptosis of photoreceptors.