%0 Journal Article
%A Timmermann, Aline
%A Tascio, Dario
%A Jabs, Ronald
%A Boehlen, Anne
%A Domingos, Catia
%A Skubal, Magdalena
%A Huang, Wenhui
%A Kirchhoff, Frank
%A Henneberger, Christian
%A Bilkei-Gorzo, Andras
%A Seifert, Gerald
%A Steinhäuser, Christian
%T Dysfunction of NG2 glial cells affects neuronal plasticity and behavior.
%J Glia
%V 71
%N 6
%@ 0894-1491
%C Bognor Regis [u.a.]
%I Wiley-Liss
%M DZNE-2023-00441
%P 1481 - 1501
%D 2023
%X 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
%K Mice
%K Animals
%K Proteoglycans: metabolism
%K Neuroglia: metabolism
%K Neurons: metabolism
%K Oligodendroglia: metabolism
%K Neuronal Plasticity
%K Antigens: metabolism
%K Kir4.1 (Other)
%K NG2 glia (Other)
%K myelination (Other)
%K neuron-glia signaling (Other)
%K neuronal plasticity (Other)
%K Proteoglycans (NLM Chemicals)
%K Antigens (NLM Chemicals)
%F PUB:(DE-HGF)16
%9 Journal Article
%$ pmid:36802096
%R 10.1002/glia.24352
%U https://pub.dzne.de/record/257561