Home > Publications Database > Dysfunction of NG2 glial cells affects neuronal plasticity and behavior. > print

001     257561
005     20231004134635.0
024 7 _ |a 10.1002/glia.24352
|2 doi
024 7 _ |a pmid:36802096
|2 pmid
024 7 _ |a 0894-1491
|2 ISSN
024 7 _ |a 1098-1136
|2 ISSN
024 7 _ |a altmetric:142818250
|2 altmetric
037 _ _ |a DZNE-2023-00441
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Timmermann, Aline
|b 0
245 _ _ |a Dysfunction of NG2 glial cells affects neuronal plasticity and behavior.
260 _ _ |a Bognor Regis [u.a.]
|c 2023
|b Wiley-Liss
336 7 _ |a article
|2 DRIVER
336 7 _ |a Output Types/Journal article
|2 DataCite
336 7 _ |a Journal Article
|b journal
|m journal
|0 PUB:(DE-HGF)16
|s 1683882733_24932
|2 PUB:(DE-HGF)
336 7 _ |a ARTICLE
|2 BibTeX
336 7 _ |a JOURNAL_ARTICLE
|2 ORCID
336 7 _ |a Journal Article
|0 0
|2 EndNote
520 _ _ |a NG2 glia represents a distinct type of macroglial cells in the CNS and is unique among glia because they receive synaptic input from neurons. They are abundantly present in white and gray matter. While the majority of white matter NG2 glia differentiates into oligodendrocytes, the physiological impact of gray matter NG2 glia and their synaptic input are still ill defined. Here, we asked whether dysfunctional NG2 glia affect neuronal signaling and behavior. We generated mice with inducible deletion of the K+ channel Kir4.1 in NG2 glia and performed comparative electrophysiological, immunohistochemical, molecular and behavioral analyses. Kir4.1 was deleted at postnatal day 23-26 (recombination efficiency about 75%) and mice were investigated 3-8 weeks later. Notably, these mice with dysfunctional NG2 glia demonstrated improved spatial memory as revealed by testing new object location recognition while working and social memory remained unaffected. Focussing on the hippocampus, we found that loss of Kir4.1 potentiated synaptic depolarizations of NG2 glia and stimulated the expression of myelin basic protein while proliferation and differentiation of hippocampal NG2 glia remained largely unaffected. Mice with targeted deletion of the K+ channel in NG2 glia showed impaired long-term potentiation at CA3-CA1 synapses, which could be fully rescued by extracellular application of a TrkB receptor agonist. Our data demonstrate that proper NG2 glia function is important for normal brain function and behavior.
536 _ _ |a 351 - Brain Function (POF4-351)
|0 G:(DE-HGF)POF4-351
|c POF4-351
|f POF IV
|x 0
588 _ _ |a Dataset connected to CrossRef, PubMed, , Journals: pub.dzne.de
650 _ 7 |a Kir4.1
|2 Other
650 _ 7 |a NG2 glia
|2 Other
650 _ 7 |a myelination
|2 Other
650 _ 7 |a neuron-glia signaling
|2 Other
650 _ 7 |a neuronal plasticity
|2 Other
650 _ 7 |a Proteoglycans
|2 NLM Chemicals
650 _ 7 |a Antigens
|2 NLM Chemicals
650 _ 2 |a Mice
|2 MeSH
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Proteoglycans: metabolism
|2 MeSH
650 _ 2 |a Neuroglia: metabolism
|2 MeSH
650 _ 2 |a Neurons: metabolism
|2 MeSH
650 _ 2 |a Oligodendroglia: metabolism
|2 MeSH
650 _ 2 |a Neuronal Plasticity
|2 MeSH
650 _ 2 |a Antigens: metabolism
|2 MeSH
700 1 _ |a Tascio, Dario
|b 1
700 1 _ |a Jabs, Ronald
|b 2
700 1 _ |a Boehlen, Anne
|b 3
700 1 _ |a Domingos, Catia
|b 4
700 1 _ |a Skubal, Magdalena
|b 5
700 1 _ |a Huang, Wenhui
|0 0000-0001-9865-0375
|b 6
700 1 _ |a Kirchhoff, Frank
|0 0000-0002-2324-2761
|b 7
700 1 _ |a Henneberger, Christian
|0 P:(DE-2719)2811625
|b 8
700 1 _ |a Bilkei-Gorzo, Andras
|0 0000-0002-6805-0472
|b 9
700 1 _ |a Seifert, Gerald
|b 10
700 1 _ |a Steinhäuser, Christian
|0 0000-0003-2579-8357
|b 11
773 _ _ |a 10.1002/glia.24352
|g Vol. 71, no. 6, p. 1481 - 1501
|0 PERI:(DE-600)1474828-9
|n 6
|p 1481 - 1501
|t Glia
|v 71
|y 2023
|x 0894-1491
856 4 _ |u https://pub.dzne.de/record/257561/files/DZNE-2023-00441%20SUP.zip
856 4 _ |u https://pub.dzne.de/record/257561/files/DZNE-2023-00441.pdf
|y OpenAccess
856 4 _ |u https://pub.dzne.de/record/257561/files/DZNE-2023-00441.pdf?subformat=pdfa
|x pdfa
|y OpenAccess
909 C O |o oai:pub.dzne.de:257561
|p openaire
|p open_access
|p VDB
|p driver
|p dnbdelivery
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 8
|6 P:(DE-2719)2811625
913 1 _ |a DE-HGF
|b Gesundheit
|l Neurodegenerative Diseases
|1 G:(DE-HGF)POF4-350
|0 G:(DE-HGF)POF4-351
|3 G:(DE-HGF)POF4
|2 G:(DE-HGF)POF4-300
|4 G:(DE-HGF)POF
|v Brain Function
|x 0
914 1 _ |y 2023
915 _ _ |a OpenAccess
|0 StatID:(DE-HGF)0510
|2 StatID
915 _ _ |a Creative Commons Attribution-NonCommercial-NoDerivs CC BY-NC-ND 4.0
|0 LIC:(DE-HGF)CCBYNCND4
|2 HGFVOC
915 _ _ |a DEAL Wiley
|0 StatID:(DE-HGF)3001
|2 StatID
|d 2022-11-08
|w ger
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1190
|2 StatID
|b Biological Abstracts
|d 2022-11-08
915 _ _ |a WoS
|0 StatID:(DE-HGF)0113
|2 StatID
|b Science Citation Index Expanded
|d 2022-11-08
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0160
|2 StatID
|b Essential Science Indicators
|d 2022-11-08
915 _ _ |a Nationallizenz
|0 StatID:(DE-HGF)0420
|2 StatID
|d 2023-08-24
|w ger
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0200
|2 StatID
|b SCOPUS
|d 2023-08-24
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0300
|2 StatID
|b Medline
|d 2023-08-24
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0199
|2 StatID
|b Clarivate Analytics Master Journal List
|d 2023-08-24
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1050
|2 StatID
|b BIOSIS Previews
|d 2023-08-24
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0150
|2 StatID
|b Web of Science Core Collection
|d 2023-08-24
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1030
|2 StatID
|b Current Contents - Life Sciences
|d 2023-08-24
915 _ _ |a JCR
|0 StatID:(DE-HGF)0100
|2 StatID
|b GLIA : 2022
|d 2023-08-24
915 _ _ |a IF >= 5
|0 StatID:(DE-HGF)9905
|2 StatID
|b GLIA : 2022
|d 2023-08-24
920 1 _ |0 I:(DE-2719)1013029
|k AG Henneberger
|l Role of astrocytes and extracellular matrix in signal transmission to the brain
|x 0
980 _ _ |a journal
980 _ _ |a VDB
980 _ _ |a I:(DE-2719)1013029
980 _ _ |a UNRESTRICTED
980 1 _ |a FullTexts

LibraryCollectionCLSMajorCLSMinorLanguageAuthor
Marc 21