J Comp Physiol B. 1993;163(7):533-40. doi: 10.1007/BF00302111.
The signal-transduction system that mediates the melanosome-aggregating response in melanophores of the black-moor goldfish, Carassius auratus, was investigated by examining the inhibition of adenylate cyclase activity mediated by α-adrenoceptors in cultured cells. When the melanophores were incubated with 1 mmol·1⁻¹ 3-isobutyl-1-methylxanthine for 5 min, the intracellular level of cyclic adenosine-3',5'-monophosphate increased two- to three-fold. Norepinephrine at 100 nmol· 1⁻¹ and naphazoline at 1 μmol· 1⁻¹ inhibited the 3-isobutyl-1-methylxanthine-induced accumulation of cyclic adenosine-3',5'-monophosphate in the cells in both the presence and the absence of isoproterenol, a beta-adrenergic agonist. Methoxamine and phenylephrine also reduced the extent of accumulation of cyclic adenosine-3',5'-monophosphate, but only when they were present at relatively high concentrations (above 100 μmol·1⁻¹). The range of concentrations at which norepinephrine inhibited the accumulation of cyclic adenosine-3',5'-monophosphate was consistent with the range at which it induced the aggregation of melanosomes. Pretreatment of the cells with pertussis toxin (1 μg·m1⁻¹) for 15 h or treatment with 100 nmol·1⁻¹ yohimbine (an α₂-adrenergic antagonist) inhibited the effects of the α-adrenergic agonists on both the aggregation of melanosomes and the 3-isobutyl-1-methylxanthine-induced accumulation of cyclic adenosine-3',5'-monophosphate, but prazosin (an α₁-adrenergic antagonist) at 100 nmol·1⁻¹ was not inhibitory. These results indicate that the melanosome-aggregating response of the goldfish melanophore is induced mainly via inhibition of the activity of adenylate cyclase,which occurs as a result of stimulation of a pathway that involves α₂-adrenoceptors and a inhibitory GTP-binding protein.
我们通过检测 α-肾上腺素受体介导的腺苷酸环化酶活性，研究了介导金鱼黑素细胞黑素体聚集反应的信号转导系统。当黑素细胞用 1mmol·1⁻¹ 3-异丁基-1-甲基黄嘌呤孵育 5 分钟时，细胞内环腺苷酸-3'，5'-单磷酸的水平增加了两到三倍。100nmol·1⁻¹ 的去甲肾上腺素和 1μmol·1⁻¹ 的萘甲唑啉在异丙肾上腺素（β-肾上腺素激动剂）存在或不存在的情况下均可抑制 3-异丁基-1-甲基黄嘌呤诱导的细胞中环腺苷酸-3'，5'-单磷酸的积累。甲氧胺和苯肾上腺素也降低了环腺苷酸-3'，5'-单磷酸的积累程度，但仅在它们存在于相对较高的浓度（高于 100μmol·1⁻¹）时。去甲肾上腺素抑制环腺苷酸-3'，5'-单磷酸积累的浓度范围与它诱导黑素体聚集的浓度范围一致。细胞用百日咳毒素（1μg·m1⁻¹）预处理 15 小时或用 100nmol·1⁻¹ 育亨宾（α₂-肾上腺素受体拮抗剂）处理，均可抑制 α-肾上腺素受体激动剂对黑素体聚集和 3-异丁基-1-甲基黄嘌呤诱导的环腺苷酸-3'，5'-单磷酸积累的影响，但 100nmol·1⁻¹ 的哌唑嗪（α₁-肾上腺素受体拮抗剂）没有抑制作用。这些结果表明，金鱼黑素细胞的黑素体聚集反应主要是通过抑制腺苷酸环化酶的活性而诱导的，这种作用是由于刺激涉及 α₂-肾上腺素受体和抑制性 GTP 结合蛋白的途径而发生的。
