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Role of protein kinase C in light adaptation of molluscan microvillar photoreceptors
Author(s) -
Piccoli Giuseppe,
Gomez Maria del Pilar,
Nasi Enrico
Publication year - 2002
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2002.022772
Subject(s) - protein kinase c , microbiology and biotechnology , biology , phorbol , stimulation , signal transduction , visual phototransduction , biophysics , biochemistry , neuroscience , retinal
The mechanisms by which Ca 2+ regulates light adaptation in microvillar photoreceptors remain poorly understood. Protein kinase C (PKC) is a likely candidate, both because some sub‐types are activated by Ca 2+ and because of its association with the macromolecular ‘light‐transduction complex’ in Drosophila . We investigated the possible role of PKC in the modulation of the light response in molluscan photoreceptors. Western blot analysis with isoform‐specific antibodies revealed the presence of PKCα in retinal homogenates. Immunocytochemistry in isolated cell preparations confirmed PKCα localization in microvillar photoreceptors, preferentially confined to the light‐sensing lobe. Light stimulation induced translocation of PKCα immunofluorescence to the photosensitive membrane, an effect that provides independent evidence for PKC activation by illumination; a similar outcome was observed after incubation with the phorbol ester PMA. Several chemically distinct activators of PKC, such as phorbol‐12‐myristate‐13‐acetate (PMA), (‐)indolactam V and 1,2,‐dioctanoyl‐ sn ‐glycerol (DOG) inhibited the light response of voltage‐clamped microvillar photoreceptors, but were ineffective in ciliary photoreceptors, in which light does not activate the G q /PLC cascade, nor elevates intracellular Ca 2+ . Pharmacological inhibition of PKC antagonized the desensitization produced by adapting lights and also caused a small, but consistent enhancement of basal sensitivity. These results strongly support the involvement of PKC activation in the light‐dependent regulation of response sensitivity. However, unlike adapting background light or elevation of [Ca 2+ ] i , PKC activators did not speed up the photoresponse, nor did PKC inhibitors antagonize the accelerating effects of background adaptation, suggesting that modulation of photoresponse time course may involve a separate Ca 2+ ‐dependent signal.