- Abstract:
-
It has been suggested that a functional deficit in NMDA-receptors (NMDARs) on parvalbumin (PV)-positive interneurons (PV-NMDARs) is central to the pathophysiology of schizophrenia. Supportive evidence come from examination of genetically modified mice where the obligatory NMDAR-subunit GluN1 (also known as NR1) has been deleted from PV interneurons by Cre-mediated knockout of the corresponding gene Grin1 (Grin1(ΔPV) mice). Notably, such PV-specific GluN1 ablation has been reported to blunt th...
Expand abstract - Publication status:
- Published
- Peer review status:
- Peer reviewed
- Version:
- Publisher's version
- Files:
-
-
(pdf, 905.4KB)
-
- Publisher copy:
- 10.1038/tp.2016.44
-
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- Publisher:
- Nature Publishing Group Publisher's website
- Journal:
- Translational Psychiatry Journal website
- Volume:
- 6
- Issue:
- 4
- Pages:
- e778
- Publication date:
- 2016-04-12
- Acceptance date:
- 2016-02-19
- DOI:
- EISSN:
-
2158-3188
- URN:
-
uuid:bc1d538e-aba4-4d68-b841-f438dadc9653
- Source identifiers:
-
616720
- Local pid:
- pubs:616720
- Paper number:
- 4
- Language:
- English
- Keywords:
- Copyright holder:
- A M Bygrave et al.
- Copyright date:
- 2016
- Notes:
- This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
Journal article
Knockout of NMDA-receptors from parvalbumin interneurons sensitizes to schizophrenia-related deficits induced by MK-801
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