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海兔胆碱能运动神经元中的多种神经肽:运动回路内在调制的证据

Multiple neuropeptides in cholinergic motor neurons of Aplysia: evidence for modulation intrinsic to the motor circuit.

作者信息

Cropper E C, Lloyd P E, Reed W, Tenenbaum R, Kupfermann I, Weiss K R

出版信息

Proc Natl Acad Sci U S A. 1987 May;84(10):3486-90. doi: 10.1073/pnas.84.10.3486.

DOI:10.1073/pnas.84.10.3486
PMID:3472218
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC304896/
Abstract

Changes in Aplysia biting responses during food arousal are partially mediated by the serotonergic metacerebral cells (MCCs). The MCCs potentiate contractions of a muscle utilized in biting, the accessory radula closer (ARCM), when contractions are elicited by stimulation of either of the two cholinergic motor neurons B15 or B16 that innervate the muscle. We have now shown that ARCM contractions may also be potentiated by peptide cotransmitters in the ARCM motor neurons. We found that motor neuron B15 contains small cardioactive peptides A and B (SCPA and SCPB)--i.e., whole B15 neurons were bioactive on the SCP-sensitive Helix heart, as were reverse-phase HPLC fractions of B15 neurons that eluted like synthetic SCPA and SCPB. Furthermore, [35S]methionine-labeled B15 peptides precisely coeluted with synthetic SCPA and SCPB. SCPB-like immunoreactivity was associated with dense-core vesicles in the soma of B15 and in neuritic varicosities and terminals in the ARCM. B16 motor neurons did not contain SCPA or SCPB but contained an unidentified bioactive peptide. RP-HPLC of [35S]methionine-labeled B16s resulted in one major peak of radioactivity that did not coelute with either SCP and which, when subject to Edman degradation, yielded [35S]methionine in positions where there is no methionine in the SCPs. Exogenously applied B16 peptide potentiated ARCM contractions elicited by stimulation of B15 or B16 neurons. Thus, in this system there appear to be two types of modulation; one type arises from the MCCs and is extrinsic to the motor system, whereas the second type arises from the motor neurons themselves and hence is intrinsic.

摘要

在食物激发过程中,海兔咬噬反应的变化部分是由5-羟色胺能的大脑后叶细胞(MCCs)介导的。当通过刺激支配辅助齿舌闭合肌(ARCM)的两个胆碱能运动神经元B15或B16中的任何一个来引发收缩时,MCCs会增强该肌肉在咬噬时的收缩。我们现在已经表明,ARCM运动神经元中的肽共递质也可能增强ARCM的收缩。我们发现运动神经元B15含有小的心脏活性肽A和B(SCPA和SCPB)——也就是说,整个B15神经元对SCP敏感的海蜗牛心脏具有生物活性,B15神经元的反相高效液相色谱馏分也具有这种活性,这些馏分的洗脱情况与合成的SCPA和SCPB相似。此外,[35S]甲硫氨酸标记的B15肽与合成的SCPA和SCPB精确共洗脱。SCPB样免疫反应性与B15胞体中的致密核心囊泡以及ARCM中的神经曲张和终末相关。B16运动神经元不含SCPA或SCPB,但含有一种未鉴定的生物活性肽。[35S]甲硫氨酸标记的B16的反相高效液相色谱产生了一个主要的放射性峰,该峰与SCP均不共洗脱,并且在进行埃德曼降解时,在SCP中没有甲硫氨酸的位置产生了[35S]甲硫氨酸。外源性应用B16肽可增强由刺激B15或B16神经元引发的ARCM收缩。因此,在这个系统中似乎存在两种调节类型;一种类型来自MCCs,是运动系统外部性的,而第二种类型来自运动神经元本身,因此是内在性的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e38/304896/b02dfabbf110/pnas00275-0416-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e38/304896/b02dfabbf110/pnas00275-0416-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e38/304896/b02dfabbf110/pnas00275-0416-a.jpg

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