Abstract
Bleaching light in vertebrate rods and strong colored light which converts a substantial fraction of rhodopsin (R) to metarhodopsin (M) in invertebrate photoreceptors both induce a prolonged excitation in the dark which desensitizes both kinds of photoreceptors for a long time in the dark. There are remarkable similarities between the characteristics of the prolonged dark excitation in both vertebrates and invertebrates: a) both are induced by pigment conversion from R. b) Both can be cut short by regeneration of R molecules, c) Both are composed of discrete events similar to photon-induced events, d) Both are accompanied by a large reduction in sensitivity to light, e) Both are localized to the illuminated area and do not spread all over the cell. A molecular mechanism is suggested to account for the prolonged dark excitation. The model suggests that when large amounts of R molecules are converted to the M state, many activated M molecules continue to be active in the dark due to lack of phosphorylation giving rise to the prolonged dark excitation. The decline of the prolonged excitation is due to phosphorylation’s turnoff of the active M molecules. The mechanisms by which excitation desensitizes the photoreceptor are still unknown, but in invertebrates part of it is mediated via an increase in intracellular free Ca2+.
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