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Exogenous expression of an allatotropin-related peptide receptor increased the membrane excitability in Aplysia neurons

DC Field Value Language
dc.contributor.authorZhang, Guo-
dc.contributor.authorGuo, Shi-Qi-
dc.contributor.authorYin, Si-Yuan-
dc.contributor.authorYuan, Wang-Ding-
dc.contributor.authorChen, Ping-
dc.contributor.authorKim, Ji-Il-
dc.contributor.authorWang, Hui-Ying-
dc.contributor.authorZhou, Hai-Bo-
dc.contributor.authorSusswein, Abraham J.-
dc.contributor.authorKaang, Bong-Kiun-
dc.contributor.authorJing, Jian-
dc.date.accessioned2022-06-21T07:08:50Z-
dc.date.available2022-06-21T07:08:50Z-
dc.date.created2022-05-24-
dc.date.issued2022-05-
dc.identifier.citationMolecular Brain, Vol.15 No.1, p. 42-
dc.identifier.issn1756-6606-
dc.identifier.urihttps://hdl.handle.net/10371/182613-
dc.description.abstractNeuropeptides act mostly on a class of G-protein coupled receptors, and play a fundamental role in the functions of neural circuits underlying behaviors. However, physiological functions of some neuropeptide receptors are poorly understood. Here, we used the molluscan model system Aplysia and microinjected the exogenous neuropeptide receptor apATRPR (Aplysia allatotropin-related peptide receptor) with an expression vector (pNEX3) into Aplysia neurons that did not express the receptor endogenously. Physiological experiments demonstrated that apATRPR could mediate the excitability increase induced by its ligand, apATRP (Aplysia allatotropin-related peptide), in the Aplysia neurons that now express the receptor. This study provides a definitive evidence for a physiological function of a neuropeptide receptor in molluscan animals.-
dc.language영어-
dc.publisherBioMed Central-
dc.titleExogenous expression of an allatotropin-related peptide receptor increased the membrane excitability in Aplysia neurons-
dc.typeArticle-
dc.identifier.doi10.1186/s13041-022-00929-4-
dc.citation.journaltitleMolecular Brain-
dc.identifier.wosid000792612600002-
dc.identifier.scopusid2-s2.0-85129571173-
dc.citation.number1-
dc.citation.startpage42-
dc.citation.volume15-
dc.description.isOpenAccessN-
dc.contributor.affiliatedAuthorKaang, Bong-Kiun-
dc.type.docTypeArticle-
dc.description.journalClass1-
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