Svensson S P, Adolfsson P I, Grundström N, Karlsson J O
Department of Pharmacology, Faculty of Health Science, Linköping University, Sweden.
Pigment Cell Res. 1997 Dec;10(6):395-400. doi: 10.1111/j.1600-0749.1997.tb00698.x.
It has previously been shown that alpha 2-adrenoceptors (alpha 2-ARs) mediate pigment granule (melanosome) aggregation in melanophores of the teleost fish Labrus ossifagus. The present investigation scrutinized the signalling mechanisms of melanosome aggregation induced by sympathetic nerve stimulation or by exogenous addition of alpha-AR agonists and cAMP analogues. The following was observed: i) nerve-induced melanosome aggregation was associated with a rapid decrease in the cAMP level; ii) noradrenaline or medetomidine (an alpha 2-AR agonist) caused melanosome aggregation and reduced the cAMP content; iii) RP-8-Cl-cAMP, a membrane-permeating inhibitor of protein kinase A induced melanosome aggregation; and iv) B-HT 920 (an alpha 2-AR agonist) and methoxamine (an alpha 1-AR agonist) induced melanosome aggregation, although they did not reduce cAMP. It has been suggested that in some teleost species alpha 1-ARs mediate melanosome aggregation by increasing the level of intracellular calcium. However, we found that the effect of methoxamine in melanophores from Labrus ossifagus could be blocked by yohimbine (an alpha 2-AR antagonist) but not by equimolar concentration of prazosin (an alpha 1-AR antagonist). Furthermore, 1 microM ionomycin (a calcium ionophore) did not induce melanosome aggregation. Our findings therefore do not indicate that alpha 1-ARs and/or an increase in intracellular calcium mediate melanosome aggregation in Labrus ossifagus. Our results suggest that alpha 2-AR-mediated melanosome aggregation is induced by multiple signalling pathways. One of these involves a reduction in cAMP, but none involves an increase in intracellular calcium.
先前的研究表明，α2 - 肾上腺素能受体（α2 - ARs）介导硬骨鱼褐菖鲉黑素细胞中色素颗粒（黑素体）的聚集。本研究详细探究了交感神经刺激或外源性添加α - AR激动剂及cAMP类似物诱导黑素体聚集的信号传导机制。结果如下：i）神经诱导的黑素体聚集与cAMP水平的快速下降有关；ii）去甲肾上腺素或美托咪定（一种α2 - AR激动剂）导致黑素体聚集并降低cAMP含量；iii）RP - 8 - Cl - cAMP，一种蛋白激酶A的膜渗透性抑制剂，诱导黑素体聚集；iv）B - HT 920（一种α2 - AR激动剂）和甲氧明（一种α1 - AR激动剂）诱导黑素体聚集，尽管它们并未降低cAMP。有人提出，在一些硬骨鱼物种中，α1 - ARs通过提高细胞内钙水平介导黑素体聚集。然而，我们发现，甲氧明对褐菖鲉黑素细胞的作用可被育亨宾（一种α2 - AR拮抗剂）阻断，但不能被等摩尔浓度的哌唑嗪（一种α1 - AR拮抗剂）阻断。此外，1 μM离子霉素（一种钙离子载体）未诱导黑素体聚集。因此，我们的研究结果并不表明α1 - ARs和/或细胞内钙的增加介导了褐菖鲉黑素体的聚集。我们的结果表明，α2 - AR介导的黑素体聚集是由多种信号通路诱导的。其中一条涉及cAMP的减少，但均不涉及细胞内钙的增加。
