000281868 001__ 281868
000281868 005__ 20251127141829.0
000281868 0247_ $$2doi$$a10.1007/s11302-025-10074-x
000281868 0247_ $$2pmid$$apmid:40024982
000281868 0247_ $$2pmc$$apmc:PMC12595207
000281868 0247_ $$2ISSN$$a1573-9538
000281868 0247_ $$2ISSN$$a1573-9546
000281868 037__ $$aDZNE-2025-01239
000281868 041__ $$aEnglish
000281868 082__ $$a540
000281868 1001_ $$00000-0002-5021-9495$$avon Mücke-Heim, Iven-Alex$$b0
000281868 245__ $$aEstablishment and behavioural characterization of a novel constitutive P2X7 receptor knockout mouse line.
000281868 260__ $$aDordrecht$$bSpringer Science + Business Media B.V.$$c2025
000281868 3367_ $$2DRIVER$$aarticle
000281868 3367_ $$2DataCite$$aOutput Types/Journal article
000281868 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1764249166_8031
000281868 3367_ $$2BibTeX$$aARTICLE
000281868 3367_ $$2ORCID$$aJOURNAL_ARTICLE
000281868 3367_ $$00$$2EndNote$$aJournal Article
000281868 520__ $$aThe P2X7 receptor is an adenosine triphosphate (ATP)-gated ion channel expressed in different cell types of the brain. Polymorphisms in the P2RX7 gene have repeatedly been associated with psychiatric disorders including major depression. Depression is a stress-related disorder in which a dysregulation of the immune system has attracted increasing attention as a potential disease mechanism. The well-documented role of P2X7 in inflammatory conditions advocates its involvement in immune system dysregulation and depression genesis. However, understanding its exact role requires further research using appropriate animal models. Unfortunately, some of the most widely used P2X7 knockout mouse models are limited in their utility by the continuous expression of certain P2rx7 splice variants or even activation of de novo transcripts. To overcome this limitation, we generated a novel constitutive and complete P2X7 KO mouse line. These KO mice lack all known murine splice variants and protein expression resulting in a loss-of-function as confirmed by calcium imaging and by the inability of P2X7-deficient peritoneal macrophages to mount an appropriate interleukin (IL)-1β response. Comprehensive characterization using a battery of tests assessing locomotion, anxiety- and depression-related as well as social behaviour revealed differences in locomotor and exploratory behaviours. P2X7 KO mice showed slightly increased locomotor activity and reduced anxiety-related behaviour at baseline. Under conditions of chronic stress exposure, genotype-dependent differences largely dissolved while P2X7 deficiency promoted enhanced stress resilience with regard to social behaviour. Taken together, our findings add further evidence for an involvement of the P2X7 in shaping different behavioural responses and their modulation by stressful environments. This novel loss-of-function model will contribute to a better understanding of P2X7 in stress-associated behaviours in basic and translational neuropsychiatric research.
000281868 536__ $$0G:(DE-HGF)POF4-352$$a352 - Disease Mechanisms (POF4-352)$$cPOF4-352$$fPOF IV$$x0
000281868 588__ $$aDataset connected to CrossRef, PubMed, , Journals: pub.dzne.de
000281868 650_7 $$2Other$$aBehaviour
000281868 650_7 $$2Other$$aKnockout mice
000281868 650_7 $$2Other$$aP2X7 receptor
000281868 650_7 $$2Other$$aP2rx7 gene
000281868 650_7 $$2Other$$aPurinergic
000281868 650_7 $$2NLM Chemicals$$aReceptors, Purinergic P2X7
000281868 650_7 $$2NLM Chemicals$$aP2rx7 protein, mouse
000281868 650_2 $$2MeSH$$aAnimals
000281868 650_2 $$2MeSH$$aReceptors, Purinergic P2X7: genetics
000281868 650_2 $$2MeSH$$aReceptors, Purinergic P2X7: metabolism
000281868 650_2 $$2MeSH$$aMice, Knockout
000281868 650_2 $$2MeSH$$aMice
000281868 650_2 $$2MeSH$$aBehavior, Animal: physiology
000281868 650_2 $$2MeSH$$aMale
000281868 650_2 $$2MeSH$$aMice, Inbred C57BL
000281868 650_2 $$2MeSH$$aDepression: genetics
000281868 650_2 $$2MeSH$$aDepression: metabolism
000281868 650_2 $$2MeSH$$aAnxiety: genetics
000281868 650_2 $$2MeSH$$aAnxiety: metabolism
000281868 650_2 $$2MeSH$$aDisease Models, Animal
000281868 650_2 $$2MeSH$$aStress, Psychological: metabolism
000281868 7001_ $$aOldekamp, Judit$$b1
000281868 7001_ $$aMetzger, Michael W$$b2
000281868 7001_ $$aKläffgen, Sarah$$b3
000281868 7001_ $$aTang, Hao$$b4
000281868 7001_ $$aWalser, Sandra M$$b5
000281868 7001_ $$aDedic, Nina$$b6
000281868 7001_ $$aRammes, Gerhard$$b7
000281868 7001_ $$00000-0002-2640-9336$$aHolsboer, Florian$$b8
000281868 7001_ $$0P:(DE-2719)2000028$$aWurst, Wolfgang$$b9
000281868 7001_ $$00000-0002-9329-5252$$aDeussing, Jan M$$b10
000281868 773__ $$0PERI:(DE-600)2172143-9$$a10.1007/s11302-025-10074-x$$gVol. 21, no. 5, p. 1077 - 1092$$n5$$p1077 - 1092$$tPurinergic signalling$$v21$$x1573-9538$$y2025
000281868 8564_ $$uhttps://pub.dzne.de/record/281868/files/DZNE-2025-01239%20SUP.docx
000281868 8564_ $$uhttps://pub.dzne.de/record/281868/files/DZNE-2025-01239.pdf$$yOpenAccess
000281868 8564_ $$uhttps://pub.dzne.de/record/281868/files/DZNE-2025-01239%20SUP.doc
000281868 8564_ $$uhttps://pub.dzne.de/record/281868/files/DZNE-2025-01239%20SUP.odt
000281868 8564_ $$uhttps://pub.dzne.de/record/281868/files/DZNE-2025-01239%20SUP.pdf
000281868 8564_ $$uhttps://pub.dzne.de/record/281868/files/DZNE-2025-01239.pdf?subformat=pdfa$$xpdfa$$yOpenAccess
000281868 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2000028$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b9$$kDZNE
000281868 9131_ $$0G:(DE-HGF)POF4-352$$1G:(DE-HGF)POF4-350$$2G:(DE-HGF)POF4-300$$3G:(DE-HGF)POF4$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lNeurodegenerative Diseases$$vDisease Mechanisms$$x0
000281868 9141_ $$y2025
000281868 915__ $$0StatID:(DE-HGF)0200$$2StatID$$aDBCoverage$$bSCOPUS$$d2025-01-06
000281868 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline$$d2025-01-06
000281868 915__ $$0StatID:(DE-HGF)1050$$2StatID$$aDBCoverage$$bBIOSIS Previews$$d2025-01-06
000281868 915__ $$0StatID:(DE-HGF)1190$$2StatID$$aDBCoverage$$bBiological Abstracts$$d2025-01-06
000281868 915__ $$0LIC:(DE-HGF)CCBY4$$2HGFVOC$$aCreative Commons Attribution CC BY 4.0
000281868 915__ $$0StatID:(DE-HGF)0100$$2StatID$$aJCR$$bPURINERG SIGNAL : 2022$$d2025-01-06
000281868 915__ $$0StatID:(DE-HGF)0113$$2StatID$$aWoS$$bScience Citation Index Expanded$$d2025-01-06
000281868 915__ $$0StatID:(DE-HGF)3002$$2StatID$$aDEAL Springer$$d2025-01-06$$wger
000281868 915__ $$0StatID:(DE-HGF)0150$$2StatID$$aDBCoverage$$bWeb of Science Core Collection$$d2025-01-06
000281868 915__ $$0StatID:(DE-HGF)9900$$2StatID$$aIF < 5$$d2025-01-06
000281868 915__ $$0StatID:(DE-HGF)0510$$2StatID$$aOpenAccess
000281868 915__ $$0StatID:(DE-HGF)0160$$2StatID$$aDBCoverage$$bEssential Science Indicators$$d2025-01-06
000281868 915__ $$0StatID:(DE-HGF)0199$$2StatID$$aDBCoverage$$bClarivate Analytics Master Journal List$$d2025-01-06
000281868 9201_ $$0I:(DE-2719)1140001$$kAG Wurst$$lGenome Engineering$$x0
000281868 980__ $$ajournal
000281868 980__ $$aVDB
000281868 980__ $$aUNRESTRICTED
000281868 980__ $$aI:(DE-2719)1140001
000281868 9801_ $$aFullTexts