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By J.L. Arpigny, J. Coyette, S. Davail, G. Feller, E. Fonze, E.C. Foulkes, J.-M. Frere, R. Fujii, S. Genicot, C. Gerday, B. Joris, J. Lamotte-Brasseur, J.N. Maina, E. Narinx, M. Nguyen-Disteche, N. Oshima, A. Vairengo, Z. Zekhnini

ADVANCES IN COMPARATIVE AND ENVIRONMENTAL body structure is helping biologists, physiologists, and biochemists retain music of the wide literature in thefield. delivering entire, built-in stories and sound, severe, and provocative summaries, this sequence is a needs to for all lively researchers in environmental and comparative body structure. the current quantity includes six reports on: - Motile actions of Fish Chromatophores. - Epithelial shipping of Heavy Metals. - Heavy steel Cytotoxicity in Marine Organisms. - Comparative Pulmonary Morphology and Morphometry. - Molecular variations in Resistance to Penicillins. - Molecular diversifications of Enzymes From Thermophilic and Psychrophilic Organisms.

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For example, Matsumoto et al. (1978) observed aggregation of pigment in erythrophores of the swordtail (Xiphophorus helleri) in primary culture. Satake (1980) detected the same effect in goldfish erythrophores after intracranial injection of the principle. Motile iridophores of neon tetras (Oshima et al. 1989) and of blue-green damselfish (Kasukawa et al. 1987) responded to the amine by the LR response. In all cases, the direction of the response was the same as that to sympathetic stimuli. Leucosomes in the leucophores of the medaka aggregated in response to melatonin (Obika 1976,1988).

Working on the medaka Oryzias latipes, Sugimoto et al. (1985) found that, even in amelanotic melanophores which lack mature melanin, dispersal of colorless premelanosomes occurred in response to MSH. Leucophores of medakas responded to MSH by the dispersion of leucosomes (Negishi and Obika 1980; Oshima and Fujii 1985). This result was rather unexpected, since leucophores normally respond to first-messenger signals in the opposite way to light-absorbing chromatophores. In some cases, such as those cited by Pickford and Atz (1957), MSH fails to disperse pigment, as has recently been confirmed.

Until the time at which the disconnected peripheral nerves lose their functions, furthermore, nervous transmitters leak out through the presynaptic membranes (cf. Sect. 2). The true transmitter, norepinephrine, soon disappears, while the adenine-derived co-transmitter, which persists for a longer time around the chromatophores, may actively cause dispersion of the dark pigment. This phenomenon lasts for about a day under normal conditions. After the functional degeneration of the axonal cylinder distal to the cut, chromatophores are mainly under the influence of MSH.

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