首页> 外文期刊>Journal of Insect Physiology >Suppression of JH biosynthesis by JH analog treatment: Mechanism of suppression and roles of allatostatins and nervous connections in the cockroach Diploptera punctata
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Suppression of JH biosynthesis by JH analog treatment: Mechanism of suppression and roles of allatostatins and nervous connections in the cockroach Diploptera punctata

机译:JH类似物抑制JH生物合成:蟑螂Diploptera punctata的抑制机制,阿托他汀和神经连接的作用

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Juvenile hormone analogs are known to inhibit the production of juvenile hormone (JH) by the corpora allata (CA). However, the mechanism of this inhibition remains undefined. We have used two JH mimics, fenoxycarb and pyriproxyfen, to examine the mechanism of suppression in the cockroach, Diploptera punctata. Denervation experiments demonstrated the importance of nervous connections between the brain and CA for the inhibition of JH biosynthesis by fenoxycarb. Fenoxycarb treatment alters the sensitivity of CA to allatostatin treatment in vitro. Suppression of JH biosynthesis by fenoxycarb following denervation of the CA showed that innervation was in part responsible for the inhibition. Similarly, maximal inhibition by Dippu-AST7 requires intact nervous connections between the brain and CA, particularly during rapid vitellogenesis. qPCR analysis of brain, CA, ovary and midgut extracts revealed that both allatostatin and its receptor Dippu-ASTR2 show increased levels of expression following topical fenoxycarb treatment, particularly in brain tissue on days 4 and 5 of the first gonadotrophic cycle and in CA on day 4. The correlation between inhibition of JH biosynthesis and increased expression of AST and ASTR2 in brains and CA, together with increased sensitivity of CA to allatostatin in vitro, suggests that allatostatin may be one of the effectors by which fenoxycarb inhibits JH biosynthesis.
机译:已知少年激素类似物会抑制体集(CA)产生少年激素(JH)。但是,这种抑制的机制仍然不确定。我们已经使用了两种JH模拟物,苯氧威和吡ip氧芬来检查蟑螂Diploptera punctata中的抑制机制。去神经实验证明了脑和CA之间神经连接对于抑制苯氧威JH生物合成的重要性。苯氧威治疗可改变CA对体外阿托伐他汀治疗的敏感性。 CA失神经后,苯氧威抑制JH生物合成表明,神经支配在一定程度上是抑制作用的原因。同样,Dippu-AST7的最大抑制作用需要大脑和CA之间完整的神经联系,尤其是在快速卵黄形成过程中。对脑,CA,卵巢和中肠提取物的qPCR分析显示,阿托他汀及其受体Dippu-ASTR2均显示出局部使用苯甲酰威芬治疗后表达水平升高,尤其是在第一个促性腺激素循环第4天和第5天以及第一天的CA中4. JH生物合成的抑制与大脑和CA中AST和ASTR2表达增加之间的相关性,以及CA在体外对allatostatin的敏感性增加,表明allatostatin可能是苯氧威克星抑制JH生物合成的效应子之一。

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