Abstract

Abstract

NG2 glia represent a distinct type of macroglial cells in the CNS and are unique among glia because they receive synaptic input from neurons. They are abundantly present in white and grey matter. While the majority of white matter NG2 glia differentiates into oligodendrocytes, the physiological impact of grey matter NG2 glia and their synaptic input are ill defined yet. 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. Focussing on the hippocampus, we found that loss of the Kir4.1 potentiated synaptic depolarizations of NG2 glia and enhanced the expression of myelin basic protein. Notably, while mice with targeted deletion of the K+ channel in NG2 glia showed impaired long term potentiation at CA3-CA1 synapses, they demonstrated improved spatial memory as revealed by testing new object location recognition. Our data demonstrate that proper NG2 glia function is critical for normal brain function and behavior.

Competing Interest Statement

The authors have declared no competing interest.

Details

Title
Dysfunction of grey matter NG2 glial cells affects neuronal plasticity and behavior
Author
Timmermann, Aline; Jabs, Ronald; Boehlen, Anne; Domingos, Catia; Skubal, Magdalena; Huang, Wenhui; Kirchhoff, Frank; Henneberger, Christian; Bilkei-Gorzo, Andras; Seifert, Gerald; Steinhäuser, Christian
University/institution
Cold Spring Harbor Laboratory Press
Section
New Results
Publication year
2021
Publication date
Aug 20, 2021
Publisher
Cold Spring Harbor Laboratory Press
ISSN
2692-8205
Source type
Working Paper
Language of publication
English
ProQuest document ID
2564147853
Copyright
© 2021. This article is published under http://creativecommons.org/licenses/by/4.0/ (“the License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.