{ "labelLang" : "hun", "responseDate" : "2024-03-29 00:26", "paging" : { "last" : true, "first" : true, "totalPages" : 1, "totalElements" : 10, "size" : 10, "number" : 1, "numberOfElements" : 10, "sort" : [ { "direction" : "DESC", "property" : "publishedYear", "ascending" : false }, { "direction" : "ASC", "property" : "firstAuthor", "ascending" : true }, { "direction" : "ASC", "property" : "mtid", "ascending" : true } ] }, "content" : [ { "otype" : "JournalArticle", "mtid" : 30437488, "status" : "APPROVED", "published" : true, "comment" : "Laboratory of Molecular Pharmacology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, 1083, Hungary \n János Szentágothai School of Neurosciences, Semmelweis University, School of PhD Studies, Budapest, 1085, Hungary \n Cited By :28 \n Export Date: 31 March 2023 \n CODEN: JNRSD \n Correspondence Address: Sperlágh, B.; Laboratory of Molecular Pharmacology, Hungary; email: sperlagh@koki.hu \n Chemicals/CAS: adenosine triphosphate, 15237-44-2, 56-65-5, 987-65-5; polyinosinic polycytidylic acid, 24939-03-5, 26301-44-0; Cytokines; P2rx7 protein, mouse; Poly I-C; Receptors, Purinergic P2X7 \n Funding details: Horizon 2020 Framework Programme, H2020, 766124 \n Funding details: Horizon 2020 \n Funding text 1: ThisstudywassupportedbyHungarianResearchandDevelopmentFundGrantK116654toB.S.,HungarianBrain Research Program 2017-1.2.1-NKP-2017-00002 to B.S., and Gedeon Richter plc. RG-IPI-2016-TP10-0012 and the European Union’s Horizon 2020 Research and Innovation Programme under the Marie Sklodowska-Curie Grant Agreement 766124. We thank Attila Köfalvi for guidance in synaptosome preparation, Flóra Gölöncsér and Berna-dett Varga for technical assistance, the Nikon Microscopy Center, and Cell Biology Center (Flow Cytometry Core Facility), Institute of Experimental Medicine of the Hungarian Academy of Sciences (Budapest, Hungary) for assistance in cytometric bead array analyses. The authors declare no competing financial interests. *G.H. and L.O. contributed equally to this work. Correspondence should be addressed to Beáta Sperlágh at sperlagh@koki.hu. https://doi.org/10.1523/JNEUROSCI.1895-18.2019 Copyright © 2019 the authors 0270-6474/19/392542-20$15.00/0 \n Funding text 2: This study was supported by Hungarian Research and Development Fund Grant K116654 to B.S., Hungarian Brain Research Program 2017-1.2.1-NKP-2017-00002 to B.S., and Gedeon Richter plc. RG-IPI-2016-TP10-0012 and the European Union’s Horizon 2020 Research and Innovation Programme under the Marie Sklodowska-Curie Grant Agreement 766124. We thank Attila Köfalvi for guidance in synaptosome preparation, Flóra Gölöncsér and Bernadett Varga for technical assistance, the Nikon Microscopy Center, and Cell Biology Center (Flow Cytometry Core Facility), Institute of Experimental Medicine of the Hungarian Academy of Sciences (Budapest, Hungary) for assistance in cytometric bead array analyses. 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We report that endogenous activation of the purinergic ion channel P2X7 (P2rx7) is necessary and sufficient to transduce MIA to autistic phenotype in male offspring. MIA induced by poly(I:C) injections to P2rx7 wild-type mouse dams elicited an autism-like phenotype in their offspring and these alterations were not observed in P2rx7 deficient mice, or following maternal treatment with a specific P2rx7 antagonist, JNJ7965567. Genetic deletion and pharmacological inhibition of maternal P2rx7s also counteracted the induction of IL-6 in the maternal plasma and fetal brain, and disrupted brain development, whilst postnatal P2rx7 inhibition alleviated behavioral and morphological alterations in the offspring. Administration of ATP to P2rx7 wild-type dams also evoked autistic phenotype, but not in knockout dams, implying that P2rx7 activation by ATP is sufficient to induce austim-like features in offspring. Our results point to maternal and offspring P2rx7s as potential therapeutic targets for the early prevention and treatment of ASD.SIGNIFICANCE STATEMENTAutism spectrum disorder (ASD) is a neurodevelopmental psychiatric disorder caused by genetic and environmental factors. Recent studies highlighted the importance of perinatal risks, in particular, maternal immune activation (MIA), showing strong association with the later emergence of ASD in the affected children. MIA could be mimicked in animal models via injection of a non-pathogenic agent poly(I:C) during pregnancy. This is the first report showing the key role of a ligand gated ion channel, the purinergic P2X7 receptor in MIA induced autism-like behavioral and biochemical features. 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