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DOI10.1073/pnas.1921123118
Secretagogin marks amygdaloid PKCδ interneurons and modulates NMDA receptor availability
Hevesi Z.; Zelena D.; Romanov R.A.; Hanics J.; Ignácz A.; Zambon A.; Pollak D.D.; Lendvai D.; Schlett K.; Palkovits M.; Harkany T.; Hökfelt T.G.M.; Alpár A.
发表日期2021
ISSN00278424
卷号118期号:7
英文摘要The perception of and response to danger is critical for an individual’s survival and is encoded by subcortical neurocircuits. The amygdaloid complex is the primary neuronal site that initiates bodily reactions upon external threat with local-circuit interneurons scaling output to effector pathways. Here, we categorize central amygdala neurons that express secretagogin (Scgn), a Ca2+sensor protein, as a subset of protein kinase Cδ (PKCδ)+ interneurons, likely “off cells.” Chemogenetic inactivation of Scgn+/PKCδ+ cells augmented conditioned response to perceived danger in vivo. While Ca2+-sensor proteins are typically implicated in shaping neurotransmitter release presynaptically, Scgn instead localized to postsynaptic compartments. Characterizing its role in the postsynapse, we found that Scgn regulates the cell-surface availability of NMDA receptor 2B subunits (GluN2B) with its genetic deletion leading to reduced cell membrane delivery of GluN2B, at least in vitro. Conclusively, we describe a select cell population, which gates danger avoidance behavior with secretagogin being both a selective marker and regulatory protein in their excitatory postsynaptic machinery. © 2021 National Academy of Sciences. All rights reserved.
英文关键词Associative learning; Calcium-binding protein; Fear conditioning; Limbic system
语种英语
来源期刊Proceedings of the National Academy of Sciences of the United States of America
文献类型期刊论文
条目标识符http://gcip.llas.ac.cn/handle/2XKMVOVA/180644
作者单位SE-NAP Research Group of Experimental Neuroanatomy and Developmental Biology, Hungarian Academy of Sciences, Budapest, H-1094, Hungary; Department of Anatomy, Semmelweis University, Budapest, H-1094, Hungary; Department of Molecular Neurosciences, Center for Brain Research, Medical University of Vienna, Vienna, A-1090, Austria; Behavioral Neurobiology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, H-1083, Hungary; Centre for Neuroscience, Szentágothai Research Centre, Institute of Physiology, Medical School, University of Pécs, Pécs, H-7624, Hungary; Neuronal Cell Biology Research Group, Department of Physiology and Neurobiology, Eötvös Loránd University, Budapest, H-1117, Hungary; Department of Neurophysiology and Neuropharmacology, Medical University of Vienna, Vienna, A-1090, Austria; Human Brain Tissue Bank and Laboratory, Semmelweis University, Budapest, H-1094, Hungary; Department of Neuroscience, Biomedicum D0776, Karolinska Institutet, Solna, SE-17165, Sweden
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Hevesi Z.,Zelena D.,Romanov R.A.,et al. Secretagogin marks amygdaloid PKCδ interneurons and modulates NMDA receptor availability[J],2021,118(7).
APA Hevesi Z..,Zelena D..,Romanov R.A..,Hanics J..,Ignácz A..,...&Alpár A..(2021).Secretagogin marks amygdaloid PKCδ interneurons and modulates NMDA receptor availability.Proceedings of the National Academy of Sciences of the United States of America,118(7).
MLA Hevesi Z.,et al."Secretagogin marks amygdaloid PKCδ interneurons and modulates NMDA receptor availability".Proceedings of the National Academy of Sciences of the United States of America 118.7(2021).
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