多巴胺及血清動素對於淡水長臂大蝦卵黃生合成影響之研究

Abstract

生物胺中，多巴胺（Dopamine ）、血清動素（Serotonin ）、正腎上腺素(Norepinephrine）、腎上腺素（（Epinephrine）及組織胺（Histamine）等，在甲殼類的生理調節上扮演主要的角色，多巴胺及血清動素會參與甲殼類多種激素之合成與釋放，進而影響生理現象及機能上之平衡，影響之激素包括甲殼類促高血糖激素（CHH）、色素變化相關激素，卵黃生成抑制激素（VIH）及脫殼抑制激素（MIH）等等。 生物物種除了維持本身的存活與成長，更需要藉由生殖繁衍種族。有關於多巴胺及血清動素調節甲殼類生理作用的研究，目前已有相當進展，大都偏重在代謝及色素調節相關之課題，但在生殖方面的探討尚嫌不足。為此，本研究以淡水長臂大蝦（Macrobrachium rosenbergii）為材料，探討多巴胺及血清動素對於甲殼類生殖生理調節上所扮演的角色及其調節途徑。 淡水蝦經由多巴胺及血清動素每四天進行注射處理，並在注射後兩天採取血淋巴，以酵素連結免疫分析法（ELISA）檢測血淋巴中卵黃前質的含量變化，結果顯示，多巴胺對於淡水長臂大蝦卵黃生成作用有抑制的現象。將多巴胺及其拮抗物依不同濃度倍數混合注射，結果顯示，多巴胺D1型受器拮抗劑（D1 receptor antagonist ）可解除多巴胺的抑制效果。至於血清動素對其卵黃生成作用確有促進的效果；然就其拮抗劑的實驗結果顯示，5-HT1 型拮抗劑及5-HT2型拮抗劑均有拮抗5-HT 的促進效果。 在剪除眼柄的處理組中，注射Dopamine後仍保有其抑制卵黃生合成的能力，間接顯示，多巴胺的抑制卵黃生成作用並未經由眼柄中 X 器官-靜竇腺複合體分泌之卵黃生成抑制素進行，但是否直接作用在肝胰臟層次上，調節卵黃生成的作用，仍有待進一步釐清；而反觀注射血清動素組，並未有促進卵黃生成之效果產生，且卵黃生合成作用進行之速率較控制組略低。由此推知，淡水長臂大蝦眼柄中的 X -器官-血竇腺複合體並未參與多巴胺的抑制作用；血清動素影響卵黃生成作用是否需經由眼柄中 X-器官-血竇腺複合體之途徑仍須進一步加以驗證。

The biogenic amines, such as dopamine, serotonin, norepinephrine, epinephrine and histamine, play important roles in the physiological regulations in crustaceans. Dopamine and serotonin are known to be involved in the synthesis and release of several neurohormones and consequently influence the physiological homeostasis and homeokinesis .The hormones known to be regulated by these catecholamines, include crustacean hyperglycemic hormone, vitellogenesis inhibiting hormone, molt inhibiting hormone, and those related to pigmentation. Organisms constantly adjust their physiological processes under the fluctuating environmental conditions not only for survival and growth, but mostly importantly for the species propagation through reproductive processes. To date, research on the actions of dopamine and serotonin are mostly concerned with the metabolism and pigmentation regulation in the crustacean species, while the involvements of these amines in the reproduction is still lacking. Therefore, the purpose of this research is to comprehand the physiological roles of dopamine and serotonin and the pathway of their actions in the freshwater giant prawn, Macrobrachium rosenbergii. The experimented prawn, both intact and bilaterally eyestalk-ablated, were injected with dopamine and serotonin (5-HT) every 4th day, and hemolymphs were extracted 2 day thereafter. The hemolymph vitellogenin was quantified by ELISA. Results indicated that dopamine depresses the vitellogenin synthesis, while serotonin on other hand, accelerated the process. Injections with the combination of these amines with respective receptor antagonists suggested that SCH23390 (dopamine D1 receptor antagonist) showed an antagonistic effect on the dopamine action, but not domperidione (dopamine D2 receptor antagonist ). Observations clearly postulated that the action of dopamine is channelled through D1 receptor. In serotonin, both DL-propanolol hydrochloride (5-HT1 receptor antagonist) and cinanserin hydrochloride (5-HT2 receptor antagonist) showed antagonistic effects on the serotonin action, which is likely channelled through both types of 5-HT receptors examined in this study. Dopamine inhibits vitellogenin synthesis in the eyestalk-ablated prawn, and this suggests that dopamine does not regulate the vitellogenesis inhibiting hormone in the X-organ sinus gland complex located in the eyestalk. With regard to serotonin actions on the eyestalk-ablated individuals, no evidence suggest any synergistic effect of serotonin with the eyestalk ablation in the acceleration of yolk synthesis. However, both dopamine and serotonin possibly act directly on the vitellogenin synthesis site, hepatopancreas. This remains to be clarified.