{'fraction_non_alphanumeric': 0.03727200634417129, 'fraction_numerical': 0.008723235527359239, 'mean_word_length': 5.538860103626943, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Signal Transduction of MCH in Melanophores of the Tilapia, Oreochromis niloticus

Abstract Using split-fin preparations of the tilapia, Oreochromis niloticus, the effects of various drugs affecting the signal transduction pathway on MCH-induced aggregation of melanosomes were examined. A phospholipase C inhibitor (neomycin sulphate), protein kinase C (PKC) inhibitors (H-7 and staurosporine), PKC activators (SC-9 and TPA) and calmodulin inhibitors (W-7 and W-5) did not block melanophore response to MCH. However, forskolin, an adenylate cyclase stimulating drug, diminished MCH-induced aggregation of melanosomes in a dose-dependent manner. In fact, intracellular concentration of cyclic AMP (cAMP) in MCH (10 nM)-treated melanophores was found to be about 54% of the control level in melanophores immersed in physiological saline. These results suggest that cAMP is the second messenger for MCH action. Since okadaic acid at 10 &mgr;M perfectly inhibited melanosome-aggregating response to MCH, the involvement of protein phosphatase 2B in the response was also implied. In addition, the effects of several drugs on NE-induced aggregation were studied, and the possible signal transduction responsible for melanosome aggregation is comparatively discussed.