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Melanophore pigment dispersion responses to agonists show two patterns of sensitivity to inhibitors of cAMP‐dependent protein kinase and protein kinase C
Author(s) -
McClintock Timothy S.,
Rising Joshua P.,
Lerner Michael R.
Publication year - 1996
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/(sici)1097-4652(199604)167:1<1::aid-jcp1>3.0.co;2-t
Subject(s) - melanophore , protein kinase a , adenylyl cyclase , protein kinase c , gs alpha subunit , biology , medicine , receptor , phospholipase c , endocrinology , second messenger system , vasoactive intestinal peptide , signal transduction , kinase , microbiology and biotechnology , chromatophore , biochemistry , neuropeptide , fishery
Melanophore pigment dispersion is a sensitive bioassay for activation of the adenylyl cyclase and phospholipase C second‐messenger pathways. The necessity of protein kinase activation in causing pigment dispersion was confirmed for eight agonists of endogenous melanophore receptors and for two transfected receptors. All agonists and receptors previously shown to elevate intracellular cAMP in melanophores—melanocyte stimulating hormone, light, (−) norepinephrine, 5‐hydroxytrptamine, and the β 2 ‐adrenergic receptor—were able to stimulate pigment dispersion in the presence of Ro31‐8220, a potent inhibitor of protein kinase C, but were blocked in the presence of H89, an inhibitor of cAMP‐dependent protein kinase. The bombesin receptor, which elevates intracellular IP 3 in melanophores, was unable to stimulate pigment dispersion in the presence of Ro31‐8220 or H89. Agonists whose mechanism of activation of pigment dispersion are unknown were also tested. Endothelin 3 responses were blocked by both H89 and Ro31‐8220, predicting coupling to phospholipase C. Vasoactive intestinal polypeptide, oxytocin, and calcitonin gene‐related peptide β responses were blocked only by H89, predicting coupling to adenylyl cyclase. © 1996 Wiley‐Liss, Inc.