TY  - JOUR
AU  - Timmermann, Aline
AU  - Tascio, Dario
AU  - Jabs, Ronald
AU  - Boehlen, Anne
AU  - Domingos, Catia
AU  - Skubal, Magdalena
AU  - Huang, Wenhui
AU  - Kirchhoff, Frank
AU  - Henneberger, Christian
AU  - Bilkei-Gorzo, Andras
AU  - Seifert, Gerald
AU  - Steinhäuser, Christian
TI  - Dysfunction of NG2 glial cells affects neuronal plasticity and behavior.
JO  - Glia
VL  - 71
IS  - 6
SN  - 0894-1491
CY  - Bognor Regis [u.a.]
PB  - Wiley-Liss
M1  - DZNE-2023-00441
SP  - 1481 - 1501
PY  - 2023
AB  - 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
KW  - Mice
KW  - Animals
KW  - Proteoglycans: metabolism
KW  - Neuroglia: metabolism
KW  - Neurons: metabolism
KW  - Oligodendroglia: metabolism
KW  - Neuronal Plasticity
KW  - Antigens: metabolism
KW  - Kir4.1 (Other)
KW  - NG2 glia (Other)
KW  - myelination (Other)
KW  - neuron-glia signaling (Other)
KW  - neuronal plasticity (Other)
KW  - Proteoglycans (NLM Chemicals)
KW  - Antigens (NLM Chemicals)
LB  - PUB:(DE-HGF)16
C6  - pmid:36802096
DO  - DOI:10.1002/glia.24352
UR  - https://pub.dzne.de/record/257561
ER  -