THE CARBACHOL-INDUCED RELEASE OF PROTHORACICOTROPIC HORMONE FROM BRAIN-CORPUS CARDIACUM-CORPUS ALLATUM COMPLEX OF THE SILKWORM, BOMBYX-MORI
THE CARBACHOL-INDUCED RELEASE OF PROTHORACICOTROPIC HORMONE FROM BRAIN-CORPUS CARDIACUM-CORPUS ALLATUM COMPLEX OF THE SILKWORM, BOMBYX-MORI
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DOI：
10.1016/0022-1910(94)90119-8
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发表时间：
1994-06-01
影响因子：
2.2
通讯作者：
AIZONO, Y
中科院分区：
文献类型：
--
作者：
SHIRAI, Y;IWASAKI, T;AIZONO, Y
在离体条件下，0.01-10 mM氨甲酰胆碱（acetylcholine，acetylcholine）能显著刺激家蚕脑-心体-咽侧体复合体（brain-CC-CA complex）释放促前胸腺激素（prothoracotropic hormone，PTTH），1 mM musucarine也能在5 min内诱导PTTH的释放，而1 mM尼古丁则无此作用。此外，5 mM阿托品（毒蕈碱拮抗剂）抑制0.1 mM卡巴胆碱诱导的PTTH释放。为了探讨毒蕈碱型乙酰胆碱受体介导的PTTH释放的信号转导，研究了磷脂酶C（PLC）抑制剂、钙调素拮抗剂和蛋白激酶C（PKC）抑制剂对0.1mM卡巴胆碱诱导的PTTH释放的影响。2-硝基-4-羧基苯基-N，N-二苯基氨基甲酸酯（NCDC：PLC抑制剂）、N-（6-氨基己基）-5-氯-1-1-萘磺酰胺（W-7：钙调蛋白拮抗剂）和calphostin C（PKC抑制剂）引起剂量依赖性抑制卡巴胆碱诱导的PTTH释放，10 μ M NCDC、500 μ M W-7和10 μ M calphostin C完全抑制PTTH释放。这些结果表明，激活磷脂酶C，随后的蛋白磷酸化的PKC和钙/钙调蛋白依赖性蛋白激酶（CaMK）参与卡巴胆碱诱导的信号转导PTTH的释放。
The in vitro release of prothoracicotropic hormone (PTTH) from brain-corpus cardiacum-corpus allatum complex (brain-CC-CA complex) of Bombyx mori was stimulated significantly with carbachol (acetylcholine agonist) in the range of 0.01-10 mM. One mM musucarine also induced the release of PTTH within 5 min, while 1 mM nicotine exerted no effect. In addition, 5 mM atropine (muscarinic antagonist) inhibited the PTTH release induced with 0.1 mM carbachol. From these results, it became apparent that the muscarinic acetylcholine receptor was associated with the release of PTTH.To explore the signal transduction mediated by the muscarinic acetylcholine receptor in the PTTH release, the effects of phospholipase C (PLC)-inhibitor, calmodulin antagonist and protein kinase C (PKC)-inhibitor on the PTTH release induced with 0.1 mM carbachol were examined. 2-nitro-4-carboxyphenyl-N,N-diphenylcalbamate (NCDC: PLC-inhibitor), N-(6-aminohexyl)-5-chloro-1-1-naphthalenesulfonamide (W-7: calmodulin antagonist) and calphostin C (PKC-inhibitor) caused dose-dependent suppression of the carbachol-induced release of PTTH, and 10 mu M NCDC, 500 mu M W-7 and 10 mu M calphostin C suppressed the release of PTTH completely. These results suggested that activation of phospholipase C, and subsequent protein phosphorylations by PKC and calcium/calmodulin dependent protein kinase (CaMK) were involved in the carbachol-induced signal transduction in the PTTH release.