Krantic S, Dube F, Quirion R, Guerrier P
Ecole Normale Supérieure, Laboratoire de Biologie Moléculaire et Cellulaire, Lyon, France.
Dev Biol. 1991 Aug;146(2):491-8. doi: 10.1016/0012-1606(91)90250-7.
Germinal vesicle breakdown (GVBD) is the first visible response of the oocyte of Spisula solidissima to the neurohormone serotonin. Pharmacological characterization of this response was performed by using 24 serotonin-related compounds. Dose-response curves were assessed by quantification of GVBD. Rank orders of potency obtained were among agonists: serotonin greater than 8-hydroxy-2-(di-N-propylamino)tetralin hydrobromide greater than 2-methyl-serotonin greater than 1-(3-trifluoromethylphenyl)piperazine; among antagonists; ritanserin ritanserin greater than ICS205930 greater than mianserin = ketanserin = propranolol greater than metoclopramide = yohimbine greater than spiperone. Various other monoaminergic compounds tested were inefficient, demonstrating the specificity of the oocyte response to serotonin. Transduction mechanisms underlying this response were then investigated. Ca2+ appeared to be involved since serotonin induced an increase in the uptake of 45Ca2+ and since it was inefficient in calcium-free sea water. The absence of synergy between serotonin and KCl suggested that both compounds use a common transduction pathway. Exposure of the oocyte to the protein kinase C activator TPA inhibited serotonin-dependent maturation. Our data thus point to an original, previously uncharacterized pharmacological profile and transduction mechanism by which serotonin induces oocyte meiosis reinitiation in Spisula solidissima.
生发泡破裂（GVBD）是硬壳蛤卵母细胞对神经激素5-羟色胺的首个可见反应。通过使用24种与5-羟色胺相关的化合物对该反应进行了药理学特征分析。通过对GVBD进行定量来评估剂量反应曲线。在激动剂中获得的效价排序为：5-羟色胺＞8-羟基-2-（二-N-丙基氨基）四氢萘氢溴酸盐＞2-甲基-5-羟色胺＞1-（3-三氟甲基苯基）哌嗪；在拮抗剂中为：利坦色林＞ICS205930＞米安色林 = 酮色林 = 普萘洛尔＞甲氧氯普胺 = 育亨宾＞螺哌隆。所测试的各种其他单胺能化合物均无效，这表明卵母细胞对5-羟色胺反应具有特异性。随后研究了该反应的转导机制。钙离子似乎参与其中，因为5-羟色胺可诱导45Ca2+摄取增加，且在无钙海水中其作用无效。5-羟色胺与氯化钾之间不存在协同作用，这表明这两种化合物使用共同的转导途径。将卵母细胞暴露于蛋白激酶C激活剂佛波酯可抑制5-羟色胺依赖性成熟。因此，我们的数据表明了一种原始的、先前未被描述的药理学特征和转导机制，通过该机制5-羟色胺可诱导硬壳蛤卵母细胞减数分裂重新启动。
