title: Impact of adolescent GluA1 AMPA receptor ablation in forebrain excitatory neurons on behavioural correlates of mood disorders.
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.
authors.affiliation: Department of Psychiatry and Psychotherapy, RG Animal Models in Psychiatry, Central Institute of Mental Health, Medical Faculty Mannheim/Heidelberg University, Heidelberg, Germany.
authors.forename: Miriam A
authors.initials: MA
authors.lastname: Vogt
authors.forename: Hasan
authors.initials: H
authors.lastname: Elkin
authors.forename: Natascha
authors.initials: N
authors.lastname: Pfeiffer
authors.forename: Rolf
authors.initials: R
authors.lastname: Sprengel
authors.forename: Peter
authors.initials: P
authors.lastname: Gass
authors.forename: Dragos
authors.initials: D
authors.lastname: Inta
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D004195:Disease Models, Animal; D005106:Exploratory Behavior / Q000502:physiology; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects / Q000235:genetics*; D006380:Helplessness, Learned; D006801:Humans; D008297:Male; D018782:Maze Learning / Q000502:physiology; D051379:Mice; D008822:Mice, Transgenic; D019964:Mood Disorders / Q000235:genetics / Q000473:pathology*; D009474:Neurons / Q000378:metabolism*; D016548:Prosencephalon / Q000378:metabolism* / Q000473:pathology; D011930:Reaction Time / Q000502:physiology; D018091:Receptors, AMPA / Q000172:deficiency* / Q000235:genetics; D013629:Tamoxifen / Q000494:pharmacology
chemical_list: D018091:Receptors, AMPA; D013629:Tamoxifen