V Haktan Ozacmak, Aida Ricardo Arrieta, Glyne U Thorington, David A Hessinger
{"title":"n -乙酰神经氨酸(NANA)激活海葵触手支撑细胞上的l型钙通道。","authors":"V Haktan Ozacmak, Aida Ricardo Arrieta, Glyne U Thorington, David A Hessinger","doi":"10.1086/715844","DOIUrl":null,"url":null,"abstract":"<p><p>AbstractSensory receptors control nematocyst discharge on sea anemone tentacles. Micromolar <i>N</i>-acetylated sugars (<i>e.g.</i>, <i>N</i>-acetyl neuraminic acid [NANA]) bind chemoreceptors on ectodermal supporting cells and predispose adjacent nematocyst discharge in response to mechanical contact <i>via</i> a cyclic adenosine monophosphate (cAMP)-dependent sensitization pathway, while higher NANA levels dose-dependently desensitize. Recent evidence implicates L-type calcium channels in desensitizing the pathway in aconitate sea anemones <i>Aiptasia pallida</i> (also known as <i>Exaiptasia diaphana</i>). We, therefore, hypothesize that NANA activates calcium influx <i>via</i> L-type calcium channels. We demonstrate a dose-dependent, NANA-activated <sup>45</sup>Ca influx into dissociated ectodermal cells isolated from <i>A. pallida</i> tentacles, with maximal influx occurring at desensitizing concentrations of NANA. The L-type calcium channel inhibitors nifedipine, diltiazem, methoxyverapamil, and cadmium blocked NANA-stimulated <sup>45</sup>Ca influx. Elevated extracellular KCl levels dose-dependently increased nifedipine-sensitive <sup>45</sup>Ca influx to implicate voltage-gated calcium channels. Forskolin, 8-bromo-cAMP, and the protein kinase A inhibitor H-8 affect NANA-stimulated calcium influx in a manner consistent with activated cAMP-dependent pathway involvement. Because NANA chemoreceptors localize to supporting cells of cnidocyte supporting cell complexes, NANA activation of <sup>45</sup>Ca influx into isolated tentacle ectodermal cells suggests that L-type calcium channels and NANA chemoreceptors co-localize to supporting cells. Indeed, a fluorescent marker of L-type calcium channels localizes to the apical ectoderm adjacent to nematocysts of live tentacles. We conclude that supporting cell chemoreceptors activate co-localized L-type calcium channels <i>via</i> a cAMP-dependent mechanism in order to initiate desensitization. We suggest that pathway desensitization may conserve nematocysts from excessive discharge during prey capture.</p>","PeriodicalId":55376,"journal":{"name":"Biological Bulletin","volume":null,"pages":null},"PeriodicalIF":2.1000,"publicationDate":"2021-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"2","resultStr":"{\"title\":\"<i>N</i>-Acetyl Neuraminic Acid (NANA) Activates L-Type Calcium Channels on Isolated Tentacle Supporting Cells of the Sea Anemone (<i>Aiptasia pallida</i>).\",\"authors\":\"V Haktan Ozacmak, Aida Ricardo Arrieta, Glyne U Thorington, David A Hessinger\",\"doi\":\"10.1086/715844\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>AbstractSensory receptors control nematocyst discharge on sea anemone tentacles. Micromolar <i>N</i>-acetylated sugars (<i>e.g.</i>, <i>N</i>-acetyl neuraminic acid [NANA]) bind chemoreceptors on ectodermal supporting cells and predispose adjacent nematocyst discharge in response to mechanical contact <i>via</i> a cyclic adenosine monophosphate (cAMP)-dependent sensitization pathway, while higher NANA levels dose-dependently desensitize. Recent evidence implicates L-type calcium channels in desensitizing the pathway in aconitate sea anemones <i>Aiptasia pallida</i> (also known as <i>Exaiptasia diaphana</i>). We, therefore, hypothesize that NANA activates calcium influx <i>via</i> L-type calcium channels. We demonstrate a dose-dependent, NANA-activated <sup>45</sup>Ca influx into dissociated ectodermal cells isolated from <i>A. pallida</i> tentacles, with maximal influx occurring at desensitizing concentrations of NANA. The L-type calcium channel inhibitors nifedipine, diltiazem, methoxyverapamil, and cadmium blocked NANA-stimulated <sup>45</sup>Ca influx. Elevated extracellular KCl levels dose-dependently increased nifedipine-sensitive <sup>45</sup>Ca influx to implicate voltage-gated calcium channels. Forskolin, 8-bromo-cAMP, and the protein kinase A inhibitor H-8 affect NANA-stimulated calcium influx in a manner consistent with activated cAMP-dependent pathway involvement. Because NANA chemoreceptors localize to supporting cells of cnidocyte supporting cell complexes, NANA activation of <sup>45</sup>Ca influx into isolated tentacle ectodermal cells suggests that L-type calcium channels and NANA chemoreceptors co-localize to supporting cells. Indeed, a fluorescent marker of L-type calcium channels localizes to the apical ectoderm adjacent to nematocysts of live tentacles. We conclude that supporting cell chemoreceptors activate co-localized L-type calcium channels <i>via</i> a cAMP-dependent mechanism in order to initiate desensitization. We suggest that pathway desensitization may conserve nematocysts from excessive discharge during prey capture.</p>\",\"PeriodicalId\":55376,\"journal\":{\"name\":\"Biological Bulletin\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":2.1000,\"publicationDate\":\"2021-10-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"2\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Biological Bulletin\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1086/715844\",\"RegionNum\":4,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2021/9/22 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q2\",\"JCRName\":\"BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biological Bulletin","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1086/715844","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2021/9/22 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"BIOLOGY","Score":null,"Total":0}
N-Acetyl Neuraminic Acid (NANA) Activates L-Type Calcium Channels on Isolated Tentacle Supporting Cells of the Sea Anemone (Aiptasia pallida).
AbstractSensory receptors control nematocyst discharge on sea anemone tentacles. Micromolar N-acetylated sugars (e.g., N-acetyl neuraminic acid [NANA]) bind chemoreceptors on ectodermal supporting cells and predispose adjacent nematocyst discharge in response to mechanical contact via a cyclic adenosine monophosphate (cAMP)-dependent sensitization pathway, while higher NANA levels dose-dependently desensitize. Recent evidence implicates L-type calcium channels in desensitizing the pathway in aconitate sea anemones Aiptasia pallida (also known as Exaiptasia diaphana). We, therefore, hypothesize that NANA activates calcium influx via L-type calcium channels. We demonstrate a dose-dependent, NANA-activated 45Ca influx into dissociated ectodermal cells isolated from A. pallida tentacles, with maximal influx occurring at desensitizing concentrations of NANA. The L-type calcium channel inhibitors nifedipine, diltiazem, methoxyverapamil, and cadmium blocked NANA-stimulated 45Ca influx. Elevated extracellular KCl levels dose-dependently increased nifedipine-sensitive 45Ca influx to implicate voltage-gated calcium channels. Forskolin, 8-bromo-cAMP, and the protein kinase A inhibitor H-8 affect NANA-stimulated calcium influx in a manner consistent with activated cAMP-dependent pathway involvement. Because NANA chemoreceptors localize to supporting cells of cnidocyte supporting cell complexes, NANA activation of 45Ca influx into isolated tentacle ectodermal cells suggests that L-type calcium channels and NANA chemoreceptors co-localize to supporting cells. Indeed, a fluorescent marker of L-type calcium channels localizes to the apical ectoderm adjacent to nematocysts of live tentacles. We conclude that supporting cell chemoreceptors activate co-localized L-type calcium channels via a cAMP-dependent mechanism in order to initiate desensitization. We suggest that pathway desensitization may conserve nematocysts from excessive discharge during prey capture.
期刊介绍:
The Biological Bulletin disseminates novel scientific results in broadly related fields of biology in keeping with more than 100 years of a tradition of excellence. The Bulletin publishes outstanding original research with an overarching goal of explaining how organisms develop, function, and evolve in their natural environments. To that end, the journal publishes papers in the fields of Neurobiology and Behavior, Physiology and Biomechanics, Ecology and Evolution, Development and Reproduction, Cell Biology, Symbiosis and Systematics. The Bulletin emphasizes basic research on marine model systems but includes articles of an interdisciplinary nature when appropriate.