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  Cre-activation in ErbB4-positive neurons of floxed Grin1/NMDA receptor mice is not associated with major behavioral impairment

Mallien, A. S., Pfeiffer, N., Vogt, M. A., Chourbaji, S., Sprengel, R., Gass, P., et al. (2021). Cre-activation in ErbB4-positive neurons of floxed Grin1/NMDA receptor mice is not associated with major behavioral impairment. Frontiers in Psychiatry, 12: 750106, pp. 1-12. doi:10.3389/fpsyt.2021.750106.

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Mallien, Anne S., Author
Pfeiffer, Natascha, Author
Vogt, Miriam A., Author
Chourbaji, Sabine, Author
Sprengel, Rolf1, Author           
Gass, Peter, Author
Inta, Dragos, Author
Affiliations:
1Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society, ou_1497704              

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Free keywords: glutamate, neurodevelopment, pharmacogenetic, neuregulin-1, schizophrenia, NMDA receptor, postadolescent
 Abstract: Extensive evidence suggests a dysfunction of the glutamate NMDA receptor (NMDAR)
in schizophrenia, a severe psychiatric disorder with putative early neurodevelopmental origins, but clinical onset mainly during late adolescence. On the other hand, pharmacological models using NMDAR antagonists and the clinical manifestation of anti-NMDAR encephalitis indicate that NMDAR blockade/hypofunction can trigger psychosis also at adult stages, without any early developmental dysfunction. Previous genetic models of NMDAR hypofunction restricted to parvalbumin-positive interneurons indicate the necessity of an early postnatal impairment to trigger schizophrenialike
abnormalities, whereas the cellular substrates of NMDAR-mediated psychosis at
adolescent/adult stages are unknown. Neuregulin 1 (NRG1) and its receptor ErbB4
represent schizophrenia-associated susceptibility factors that closely interact with NMDAR. To determine the neuronal populations implicated in “late” NMDAR-driven psychosis, we analyzed the effect of the inducible ablation of NMDARs in ErbB4-
expressing cells in mice during late adolescence using a pharmacogenetic approach. Interestingly, the tamoxifen-inducible NMDAR deletion during this late developmental stage did not induce behavioral alterations resembling depression, schizophrenia or anxiety. Our data indicate that post-adolescent NMDAR deletion, even in a wider cell population than parvalbumin-positive interneurons, is also not sufficient to generate behavioral abnormalities resembling psychiatric disorders. Other neuronal substrates that have to be revealed by future studies, may underlie post-adolescent NMDAR-driven psychosis.

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Language(s): eng - English
 Dates: 2021-07-302021-10-272021-11-25
 Publication Status: Published online
 Pages: 11
 Publishing info: -
 Table of Contents: -
 Rev. Type: Peer
 Identifiers: DOI: 10.3389/fpsyt.2021.750106
 Degree: -

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Title: Frontiers in Psychiatry
  Abbreviation : Front Psychiatry
Source Genre: Journal
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Publ. Info: Lausanne, Switzerland : Frontiers Research Foundation
Pages: - Volume / Issue: 12 Sequence Number: 750106 Start / End Page: 1 - 12 Identifier: ISSN: 1664-0640
CoNE: https://pure.mpg.de/cone/journals/resource/16640640