Cellular signalling of PCH-induced pigment aggregation in the crustacean Macrobrachium potiuna erythrophores.

The cellular system responsible for the transduction of the pigment-concentrating hormone (PCH) signal was investigated in erythrophores of the freshwater shrimp, Macrobrachium potiuna. Dose-response curves to the hormone were determined in the absence and in the presence of several drugs that affect sequential steps of the Ca(2+)-dependent signalling pathway. Additionally, the ability of forskolin to induce pigment dispersion was evaluated. Neomycin sulphate (10(-4) and 10(-3) mol.l-1), trifluoperazine (10(-5) and 10(-4) mol.l-1), 1-(5-isoquinolinesulfonlyl)-2-methylpiperazine (10(-7) and 10(-5) mol.l-1) and okadaic acid (10(-7) mol.l-1) significantly (P < 0.05) decreased the responses to PCH. However, okadaic acid at low concentration (10(-9) mol.l-1) and cyclosporin A (10(-6) and 10(-5) mol.l-1) did not significantly (P > 0.05) affect PCH activity. Forskolin (10(-4) mol.l-1) was able to half-maximally reverse the hormone-induced aggregation. Our results suggest that the pigment-concentrating hormone induces pigment aggregation through a Ca(2+)-dependent pathway with a posteriori phosphatase activation, probably the serine/threonine phosphatase 1.