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

Vogt , Miriam A.; Elkin, Hasan; Pfeiffer, Natascha; Sprengel, Rolf; Gass, Peter; Inta, Dragos

doi:10.1007/s00406-014-0509-5

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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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Sprengel, Rolf
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Citation

Vogt, M. A., Elkin, H., Pfeiffer, N., Sprengel, R., Gass, P., & Inta, D. (2014). Impact of adolescent GluA1 AMPA receptor ablation in forebrain excitatory neurons on behavioural correlates of mood disorders. European Archives of Psychiatry and Clinical Neuroscience, 264(7), 625-629. doi:10.1007/s00406-014-0509-5.

Cite as: https://hdl.handle.net/11858/00-001M-0000-0023-C8B9-2

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.