In summary: Light closes cGMP-gated sodium channels, reducing the influx of both Na and Ca ions. Stopping the influx of Na ions effectively switches off the dark current. Reducing this dark current causes the photoreceptor to hyperpolarise, which reduces glutamate release which thus reduces the inhibition of retinal nerves, leading to excitation of these nerves. This reduced Ca influx during phototransduction enables deactivation and recovery from phototransduction, as discussed below in .
# A photon interacts with a retinal molecule in an opsin complex in a photoreceptor cell. The retinal undergoes isomerisation, changing from the 11-cis-retinal to the all-trans-retinal configuration.
# Opsin therefore undergoes a conformational change to metarhodopsin II.
# Metarhodopsin II activates a G protein known as transducin. This causes transducin to dissociate from its bound GDP, and bind GTP; then the alpha subunit of transducin dissociates from the beta and gamma subunits, with the GTP still bound to the alpha subunit.
# The alpha subunit-GTP complex activates phosphodiesterase, also known as PDE6. It binds to one of two regulatory subunits of PDE (which itself is a tetramer) and stimulates its activity. 
# PDE hydrolyzes cGMP, forming GMP. This lowers the intracellular concentration of cGMP and therefore the sodium channels close.
# Closure of the sodium channels causes hyperpolarization of the cell due to the ongoing efflux of potassium ions.
# Hyperpolarization of the cell causes voltage-gated calcium channels to close.
# As the calcium level in the photoreceptor cell drops, the amount of the neurotransmitter glutamate that is released by the cell also drops. This is because calcium is required for the glutamate-containing vesicles to fuse with cell membrane and release their contents (see SNARE proteins).
# A decrease in the amount of glutamate released by the photoreceptors causes depolarization of on-center bipolar cells (rod and cone On bipolar cells) and hyperpolarization of cone off-center bipolar cells.