English
 
User Manual Privacy Policy Disclaimer Contact us
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

Long-term NR2B expression in the cerebellum alters granule cell development and leads to NR2A down-regulation and motor deficits

MPS-Authors
/persons/resource/persons124409

Steigerwald,  Frank
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

/persons/resource/persons93955

Köhr,  Georg
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

Fulltext (public)
There are no public fulltexts available
Supplementary Material (public)
There is no public supplementary material available
Citation

Schlett, K., Pieri, I., Metzger, F., Marchetti, L., Steigerwald, F., Dere, E., et al. (2004). Long-term NR2B expression in the cerebellum alters granule cell development and leads to NR2A down-regulation and motor deficits. Cellular and Molecular Neurobiology, 27(3), 215-226. doi:10.1016/j.mcn.2004.05.008.


Cite as: http://hdl.handle.net/11858/00-001M-0000-002A-39BA-1
Abstract
N−methyl−D−aspartate receptor (NMDAR) composition in granule cells changes characteristically during cerebellar development. To analyze the importance of NR2B replacement by NR2C and NR2A subunits until the end of the first month of age, we generated mice with lasting NR2B expression but deficiency for NR2C (NR2C−2B mice). Mutant phenotype was different from NR2C knock−out mice as loss of granule cells and morphological changes in NR2C/2B cerebellar architecture were already evident from the second postnatal week. Increased NR2B subunit levels led also to a gradual down−regulation of cerebellar NR2A levels, preceding the development of motor impairment in adult animals. Therefore, cerebellar NR2A is important for proper motor coordination and cannot be replaced by long−term expression of NR2B. Consequently, the physiological exchange of NMDA receptor subunits during cerebellar granule cell maturation is important for accurate postnatal development and function