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  Dysregulated expression of Neuregulin-1 by cortical pyramidal neurons disrupts synaptic plasticity.

Agarwal, A., Zhang, M., Trembak-Duff, I., Unterbarnscheidt, T., Radyushkin, K., Dibaj, P., et al. (2014). Dysregulated expression of Neuregulin-1 by cortical pyramidal neurons disrupts synaptic plasticity. Cell Reports, 8(4), 1130-1145. doi:10.1016/j.celrep.2014.07.026.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-0023-EC12-1 Version Permalink: http://hdl.handle.net/11858/00-001M-0000-0027-CBDD-2
Genre: Journal Article

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 Creators:
Agarwal, A., Author
Zhang, M., Author
Trembak-Duff, I., Author
Unterbarnscheidt, T., Author
Radyushkin, K., Author
Dibaj, P., Author
de Souza, D. M., Author
Boretius, S.1, Author              
Brzózka, M. M., Author
Steffens, H.2, Author              
Berning, S.2, Author              
Teng, Z., Author
Gummert, M. N., Author
Tantra, M., Author
Guest, P. C., Author
Willig, K. I.2, Author              
Frahm, J.1, Author              
Hell, S. W.2, Author              
Bahn, S., Author
Rossner, M. J., Author
Nave, K. A., AuthorEhrenreich, H., AuthorZhang, W., AuthorSchwab, M. H., Author more..
Affiliations:
1Biomedical NMR Research GmbH, MPI for biophysical chemistry, Max Planck Society, ou_578634              
2Department of NanoBiophotonics, MPI for biophysical chemistry, Max Planck Society, ou_578627              

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 Abstract: Neuregulin-1 (NRG1) gene variants are associated with increased genetic risk for schizophrenia. It is unclear whether risk haplotypes cause elevated or decreased expression of NRG1 in the brains of schizophrenia patients, given that both findings have been reported from autopsy studies. To study NRG1 functions in vivo, we generated mouse mutants with reduced and elevated NRG1 levels and analyzed the impact on cortical functions. Loss of NRG1 from cortical projection neurons resulted in increased inhibitory neurotransmission, reduced synaptic plasticity, and hypoactivity. Neuronal overexpression of cysteine-rich domain (CRD)-NRG1, the major brain isoform, caused unbalanced excitatory-inhibitory neurotransmission, reduced synaptic plasticity, abnormal spine growth, altered steady-state levels of synaptic plasticity-related proteins, and impaired sensorimotor gating. We conclude that an “optimal” level of NRG1 signaling balances excitatory and inhibitory neurotransmission in the cortex. Our data provide a potential pathomechanism for impaired synaptic plasticity and suggest that human NRG1 risk haplotypes exert a gain-of-function effect.

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Language(s): eng - English
 Dates: 2014-08-142014-08-21
 Publication Status: Published in print
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 Rev. Method: Peer
 Identifiers: DOI: 10.1016/j.celrep.2014.07.026
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Title: Cell Reports
Source Genre: Journal
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Pages: - Volume / Issue: 8 (4) Sequence Number: - Start / End Page: 1130 - 1145 Identifier: -