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Impact of adolescent GluA1 AMPA receptor ablation in forebrain excitatory neurons on behavioural correlates of mood disorders

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Abstract

Glutamatergic dysfunctions have recently been postulated to play a considerable role in mood disorders. However, molecular mechanisms underlying these effects have been poorly deciphered. Previous work demonstrated the contribution of GluA1-containing AMPA receptors (AMPAR) to a depression-like and anxiety-like phenotype. Here we investigated the effect of temporally and spatially restricted gene manipulation of GluA1 on behavioural correlates of mood disorders in mice. Here we show that tamoxifen-induced GluA1 deletion restricted to forebrain glutamatergic neurons of post-adolescent mice does not induce depression- and anxiety-like changes. This differs from the phenotype of mice with global AMPAR deletion suggesting that for mood regulation AMPAR may be particularly important on inhibitory interneurons or already early in development.

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Acknowledgments

This work was supported by Deutsche Forschungsgemeinschaft (GA427/11-1) to P.G. and D.I. and the Collaborative Research Center (Sonderforschungsbereich) 636 of the University of Heidelberg to P.G.

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The authors declare that they have no conflict of interest.

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Correspondence to Dragos Inta.

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Peter Gass and Dragos Inta have contributed equally to this work.

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Vogt, M.A., Elkin, H., Pfeiffer, N. et al. Impact of adolescent GluA1 AMPA receptor ablation in forebrain excitatory neurons on behavioural correlates of mood disorders. Eur Arch Psychiatry Clin Neurosci 264, 625–629 (2014). https://doi.org/10.1007/s00406-014-0509-5

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  • DOI: https://doi.org/10.1007/s00406-014-0509-5

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