000283021 001__ 283021
000283021 005__ 20251222094330.0
000283021 0247_ $$2doi$$a10.1016/j.pneurobio.2025.102856
000283021 0247_ $$2pmid$$apmid:41297659
000283021 0247_ $$2ISSN$$a0301-0082
000283021 0247_ $$2ISSN$$a1873-5118
000283021 037__ $$aDZNE-2025-01433
000283021 041__ $$aEnglish
000283021 082__ $$a610
000283021 1001_ $$aBohmbach, Kirsten$$b0
000283021 245__ $$aGlycine and glycine transport control dendritic excitability and spiking.
000283021 260__ $$aJena$$bElsevier$$c2025
000283021 3367_ $$2DRIVER$$aarticle
000283021 3367_ $$2DataCite$$aOutput Types/Journal article
000283021 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1766392884_14400
000283021 3367_ $$2BibTeX$$aARTICLE
000283021 3367_ $$2ORCID$$aJOURNAL_ARTICLE
000283021 3367_ $$00$$2EndNote$$aJournal Article
000283021 520__ $$aNeuronal dendrites integrate excitatory input. They can perform local computations such as coincidence detection by amplifying synchronized local input and dendritic spiking. Extracellular glycine could be a powerful modulator of such processes through its action as a co-agonist at glutamate receptors of the N-methyl-D-aspartate (NMDA) subtype but also as a ligand of inhibitory glycine receptors (GlyRs). Similarly, glycine transporters (GlyTs), an emerging drug target for psychiatric and other diseases, could control dendritic integration through ambient glycine levels. Both hypotheses were tested at dendrites of CA1 pyramidal cells in acute hippocampal slices by pharmacologically analysing how glycine, GlyTs and GlyRs change the postsynaptic response to local dendritic excitatory input. Using microiontophoretic glutamate application, we found that glycine can indeed significantly increase dendritic excitability and dendritic spiking. We also uncovered that GlyTs are powerful modulators of dendritic spiking, which can limit the impact of glycine sources on CA1 pyramidal cells. Our experiments also revealed that GlyRs can have an opposite, inhibitory effect on the slow dendritic spike component. This directly demonstrates that glycine can dynamically enhance dendritic responsiveness to local input and promote dendritic spiking, while GlyTs and GlyRs have an opposing effect. Together, this makes glycinergic signalling a powerful modulator of the nonlinear integration of synaptic input in CA1 radial oblique dendrites.
000283021 536__ $$0G:(DE-HGF)POF4-351$$a351 - Brain Function (POF4-351)$$cPOF4-351$$fPOF IV$$x0
000283021 588__ $$aDataset connected to CrossRef, PubMed, , Journals: pub.dzne.de
000283021 650_7 $$2Other$$aD-serine
000283021 650_7 $$2Other$$aDendritic excitability
000283021 650_7 $$2Other$$aDendritic spiking
000283021 650_7 $$2Other$$aGlycine
000283021 650_7 $$2Other$$aGlycine transport
000283021 650_7 $$2Other$$aHippocampus
000283021 650_7 $$2Other$$aN-methyl-D-aspartate receptors
000283021 7001_ $$aBauer, Vincent$$b1
000283021 7001_ $$0P:(DE-2719)2811625$$aHenneberger, Christian$$b2$$eLast author$$udzne
000283021 773__ $$0PERI:(DE-600)1500673-6$$a10.1016/j.pneurobio.2025.102856$$gVol. 256, p. 102856 -$$p102856$$tProgress in neurobiology$$v256$$x0301-0082$$y2025
000283021 8564_ $$uhttps://pub.dzne.de/record/283021/files/DZNE-2025-1433.pdf$$yRestricted
000283021 8564_ $$uhttps://pub.dzne.de/record/283021/files/DZNE-2025-1433.pdf?subformat=pdfa$$xpdfa$$yRestricted
000283021 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2811625$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b2$$kDZNE
000283021 9131_ $$0G:(DE-HGF)POF4-351$$1G:(DE-HGF)POF4-350$$2G:(DE-HGF)POF4-300$$3G:(DE-HGF)POF4$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lNeurodegenerative Diseases$$vBrain Function$$x0
000283021 915__ $$0StatID:(DE-HGF)0420$$2StatID$$aNationallizenz$$d2024-12-10$$wger
000283021 915__ $$0StatID:(DE-HGF)0200$$2StatID$$aDBCoverage$$bSCOPUS$$d2024-12-10
000283021 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline$$d2024-12-10
000283021 915__ $$0StatID:(DE-HGF)0199$$2StatID$$aDBCoverage$$bClarivate Analytics Master Journal List$$d2024-12-10
000283021 915__ $$0StatID:(DE-HGF)1050$$2StatID$$aDBCoverage$$bBIOSIS Previews$$d2024-12-10
000283021 915__ $$0StatID:(DE-HGF)0160$$2StatID$$aDBCoverage$$bEssential Science Indicators$$d2024-12-10
000283021 915__ $$0StatID:(DE-HGF)1030$$2StatID$$aDBCoverage$$bCurrent Contents - Life Sciences$$d2024-12-10
000283021 915__ $$0StatID:(DE-HGF)1120$$2StatID$$aDBCoverage$$bBIOSIS Reviews Reports And Meetings$$d2024-12-10
000283021 915__ $$0StatID:(DE-HGF)0113$$2StatID$$aWoS$$bScience Citation Index Expanded$$d2024-12-10
000283021 915__ $$0StatID:(DE-HGF)0150$$2StatID$$aDBCoverage$$bWeb of Science Core Collection$$d2024-12-10
000283021 915__ $$0StatID:(DE-HGF)0100$$2StatID$$aJCR$$bPROG NEUROBIOL : 2022$$d2024-12-10
000283021 915__ $$0StatID:(DE-HGF)0600$$2StatID$$aDBCoverage$$bEbsco Academic Search$$d2024-12-10
000283021 915__ $$0StatID:(DE-HGF)0030$$2StatID$$aPeer Review$$bASC$$d2024-12-10
000283021 915__ $$0StatID:(DE-HGF)9905$$2StatID$$aIF >= 5$$bPROG NEUROBIOL : 2022$$d2024-12-10
000283021 9201_ $$0I:(DE-2719)1013029$$kAG Henneberger$$lSynaptic and Glial Plasticity$$x0
000283021 980__ $$ajournal
000283021 980__ $$aEDITORS
000283021 980__ $$aVDBINPRINT
000283021 980__ $$aI:(DE-2719)1013029
000283021 980__ $$aUNRESTRICTED