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昆虫肽能神经元中递质可塑性的激素调控。II. 保幼激素对羽化激素表达上调的调控

Hormonal control of transmitter plasticity in insect peptidergic neurons. II. Steroid control of the up-regulation of bursicon expression.

作者信息

Tublitz N J, Loi P K

机构信息

Institute of Neuroscience, University of Oregon, Eugene 97403.

出版信息

J Exp Biol. 1993 Aug;181:195-212. doi: 10.1242/jeb.181.1.195.

DOI:10.1242/jeb.181.1.195
PMID:8105019
Abstract

Each abdominal ganglion of the central nervous system of the tobacco hawkmoth, Manduca sexta contains four individually identified lateral neurosecretory cells (LNCs) that undergo a postembryonic transmitter switch in vivo. In the embryonic and caterpillar stages, the primary LNC transmitter is cardioacceleratory peptide 2 (CAP2), a myoregulatory peptide. During metamorphosis, these cells stop expressing CAP2 and instead produce bursicon, a classic insect peptide hormone responsible for cuticular tanning. We have previously reported that this transmitter plasticity is under the control of the insect steroid hormone 20-hydroxyecdysone (20-HE), which surges twice during the last larval instar. In that report we showed that the CAP2 decline is indirectly regulated by the first 20-HE rise, the commitment pulse (CP). Here we provide evidence that the rise in bursicon levels in the LNCs is directly triggered by the second 20-HE surge, the prepupal peak (PP). We performed several experimental manipulations that exposed LNCs to the PP without the CP; cells treated in this manner exhibited a significant rise in bursicon content. In contrast, bursicon levels remained unchanged in those LNCs exposed only to the CP. Exposure to the PP triggered a precocious increase in bursicon expression in LNCs from the penultimate larval stage. Increased bursicon levels in the LNCs were also induced by direct infusion of 20-HE. Taken together, the results of these experiments suggest that the rise in bursicon in the LNCs during metamorphosis is due to the direct action of the PP on the LNCs. Thus, the two 20-HE surges combine to regulate the CAP2-to-bursicon switch in the LNCs, the first acting indirectly to cause a decline in CAP2 levels and the second triggering a rise in bursicon expression, possibly by a direct action on the LNCs.

摘要

烟草天蛾(烟草天蛾)中枢神经系统的每个腹神经节都包含四个可单独识别的外侧神经分泌细胞(LNCs),这些细胞在体内会经历胚胎后递质转换。在胚胎期和毛虫阶段,主要的LNC递质是心加速肽2(CAP2),一种肌调节肽。在变态过程中,这些细胞停止表达CAP2,转而产生羽化激素,一种负责表皮鞣化的经典昆虫肽激素。我们之前曾报道,这种递质可塑性受昆虫类固醇激素20-羟基蜕皮激素(20-HE)的控制,20-HE在最后一龄幼虫期会激增两次。在该报告中,我们表明CAP2的下降是由第一次20-HE激增即变态决定脉冲(CP)间接调节的。在此,我们提供证据表明,LNCs中羽化激素水平的上升是由第二次20-HE激增即化蛹前峰值(PP)直接触发的。我们进行了多项实验操作,使LNCs暴露于PP但不暴露于CP;以这种方式处理的细胞羽化激素含量显著上升。相比之下,仅暴露于CP的那些LNCs中羽化激素水平保持不变。暴露于PP会引发倒数第二龄幼虫期LNCs中羽化激素表达的早熟增加。直接注入20-HE也会诱导LNCs中羽化激素水平升高。综合来看,这些实验结果表明,变态过程中LNCs中羽化激素的上升是由于PP对LNCs的直接作用。因此,两次20-HE激增共同调节LNCs中从CAP2到羽化激素的转换,第一次间接作用导致CAP2水平下降,第二次可能通过对LNCs的直接作用触发羽化激素表达的上升。

相似文献

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Hormonal control of transmitter plasticity in insect peptidergic neurons. II. Steroid control of the up-regulation of bursicon expression.昆虫肽能神经元中递质可塑性的激素调控。II. 保幼激素对羽化激素表达上调的调控
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Hormonal control of transmitter plasticity in insect peptidergic neurons. I. Steroid regulation of the decline in cardioacceleratory peptide 2 (CAP2) expression.昆虫肽能神经元中递质可塑性的激素调控。I. 类固醇对促心肽2(CAP2)表达下降的调节。
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Postembryonic alteration of transmitter phenotype in individually identified peptidergic neurons.在个体识别的肽能神经元中,胚胎后期递质表型的改变。
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The regulation of transmitter expression in postembryonic lineages in the moth Manduca sexta. I. Transmitter identification and developmental acquisition of expression.烟草天蛾胚胎后期谱系中神经递质表达的调控。I. 神经递质的鉴定及表达的发育获得
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