"Dopamine is uncouples horizontal cells both by reducing the open probabillity of the intercellular channels and by decreasing the density of connexons in the gap junction (reviewed by Negishi et al., 1990..." Vaney (1994)
There are dopaminergic amacrines which may modulate the gap junctions joining adjacent AII amacrines. (Pourcho, 1982; Sterling, 1983, Voigt and Wassle, 1987 as cited by Vaney, 1994)
In Rhesus monkey, Nguyen-Legros et al. (1990) found that dopaminergic Innerplexiform cells have terminals in the photoreceptor layer which do not make a clear conventional synapse. The purpose of these terminals is unknown, but leads to the speculation (by me) of cone gap junction modulation.
Affect of light on dopaminergic receptors
There is a variety of evidence which suggests that dopamine release is high in light. "Consequently, in the dark, when dopamine release is low, D1 receptor activity may exhibit supersensitivity." Witkovsky and Dearry
"...changes in D2 receptor number may require longer periods of light or dark adaptation." Witkovsky and Dearry
Affect of light on creation of Dopamine
One step in the creation of Dopamine is the hydroxylation of the phenol ring of tyrosine by tyrosine hydroxylase (TH).
In the Rat
Dopamine synthesis is significantly enhanced withing 60 seconds of light onset
Dopamine synthesis returns to dark levels within 10 minutes of light offset.
Iuvone et al., 1978; Proll and Morgan, 1982 as cited by Witkovsky and Dearry
Stimulation of these receptors enhances cAMP formation
Stimulation of these receptors inhibits or has no effect on adenylyl cyclase activity. (Niznik, 1987 as cited in Witkovsky and Dearry)
These have been shown to exist in human retina: McGonigle et al., 1988