In-vivo administration of clozapine affects behaviour but does not reverse dendritic spine deficits in the 14-3-3ζ KO mouse model of schizophrenia-like disorders

Jaehne, Emily J.; Ramshaw, Hayley S.; Xu, Xiang; Saleh, Eiman; Clark, Scott; Schubert, Klaus Oliver; Lopez, Angel F.; Schwarz, Quenten; Baune, Bernhard T.

doi:10.1016/j.pbb.2015.09.006

Cited by 14 publications

(13 citation statements)

References 65 publications

(82 reference statements)

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“…In the 14-3-3 FKO mice, there is a reduction of both dendritic complexity and spine density in the cortical and hippocampal neurons where the 14-3-3 inhibitor is extensively expressed [ 53 ]. A similar reduction in dendritic spine density was observed in 14-3-3 ζ -deficient mice in BALB/c background [ 54 , 55 ]. On the contrary, overexpressing 14-3-3 ζ in rat hippocampal neurons significantly increases spine density [ 56 ].…”

Section: Functions Of 14-3-3 At the Postsynaptic Sitesupporting

confidence: 67%

“…Cofilin is a major actin depolymerizing factor. Reduction of p-cofilin enhances the activity of cofilin, promotes the turnover of actin filaments, and consequently destabilizes dendritic spines [ 55 , 56 ]. Moreover, a different group identified cofilin and its regulatory kinase LIM-kinase 1 (LIMK1) as binding partners of 14-3-3 ζ and suggested that interactions with the C-terminal region of 14-3-3 ζ inhibit the binding of cofilin to F-actin [ 59 ].…”

Section: Functions Of 14-3-3 At the Postsynaptic Sitementioning

confidence: 99%

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14-3-3 Proteins in Glutamatergic Synapses

Zhang

Zhou

2018

Neural Plasticity

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The 14-3-3 proteins are a family of proteins that are highly expressed in the brain and particularly enriched at synapses. Evidence accumulated in the last two decades has implicated 14-3-3 proteins as an important regulator of synaptic transmission and plasticity. Here, we will review previous and more recent research that has helped us understand the roles of 14-3-3 proteins at glutamatergic synapses. A key challenge for the future is to delineate the 14-3-3-dependent molecular pathways involved in regulating synaptic functions.

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Section: Functions Of 14-3-3 At the Postsynaptic Sitesupporting

confidence: 67%

Section: Functions Of 14-3-3 At the Postsynaptic Sitementioning

confidence: 99%

14-3-3 Proteins in Glutamatergic Synapses

Zhang

Zhou

2018

Neural Plasticity

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“…A number of studies have shown an association between the 14-3-3ζ isoform and the development of schizophrenia, with 14-3-3ζ knockout mice becoming a model for schizophrenia (Jia et al, 2004 ; Middleton et al, 2005 ; Cheah et al, 2012 ; Fromer et al, 2014 ). More recently it has also been found that knocking out 14-3-3ζ in mice results in brain morphological changes, including a decrease in hippocampal dendritic spine density (Jaehne et al, 2015 ; Xu et al, 2015 ). In 2015, using 14-3-3ζ knockout mice, Jaehne et al ( 2015 ) found that these mice have a significant decrease in dendritic spine density in the cornu ammonis layer 3 (CA3) of the hippocampus (Jaehne et al, 2015 ).…”

Section: Neuromorphogenesis and Synaptogenesismentioning

confidence: 99%

“…More recently it has also been found that knocking out 14-3-3ζ in mice results in brain morphological changes, including a decrease in hippocampal dendritic spine density (Jaehne et al, 2015 ; Xu et al, 2015 ). In 2015, using 14-3-3ζ knockout mice, Jaehne et al ( 2015 ) found that these mice have a significant decrease in dendritic spine density in the cornu ammonis layer 3 (CA3) of the hippocampus (Jaehne et al, 2015 ). Furthermore, Xu et al ( 2015 ) generated a 14-3-3ζ knockout mouse model with a BALB/c background and found that these mice have enlarged lateral ventricles, aberrant mossy fiber connectivity and reduced synaptic density in all of the subfields of the hippocampus (Xu et al, 2015 ).…”

Section: Neuromorphogenesis and Synaptogenesismentioning

confidence: 99%

14-3-3 Proteins in Brain Development: Neurogenesis, Neuronal Migration and Neuromorphogenesis

Cornell

Toyo-oka

2017

Front. Mol. Neurosci.

116

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The 14-3-3 proteins are a family of highly conserved, multifunctional proteins that are highly expressed in the brain during development. Cumulatively, the seven 14-3-3 isoforms make up approximately 1% of total soluble brain protein. Over the last decade, evidence has accumulated implicating the importance of the 14-3-3 protein family in the development of the nervous system, in particular cortical development, and have more recently been recognized as key regulators in a number of neurodevelopmental processes. In this review we will discuss the known roles of each 14-3-3 isoform in the development of the cortex, their relation to human neurodevelopmental disorders, as well as the challenges and questions that are left to be answered. In particular, we focus on the 14-3-3 isoforms and their involvement in the three key stages of cortical development; neurogenesis and differentiation, neuronal migration and neuromorphogenesis and synaptogenesis.

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“…In fact, in the case of the ξ and ε, their deficient mice show abnormal behavioral patterns that show symptoms of disease. The 14-3-3ξ-deficient mice exhibit neuropsychiatric behaviors, cognitive defects, and hyperactivity locomotion ( 131 - 133 ). The 14-3-3ε-deficient mice showed schizophrenia-like behavior, hyperactive loco-motion, and working memory defect ( 134 , 135 ).…”

Section: Discussionmentioning

confidence: 99%

Emerging roles of 14-3-3γ in the brain disorder

Cho

Park

2020

BMB Rep.

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14-3-3 proteins are mostly expressed in the brain and are closely involved in numerous brain functions and various brain disorders. Among the isotypes of the 14-3-3 proteins, 14-3-3γ is mainly expressed in neurons and is highly produced during brain development, which could indicate that it has a significance in neural development. Furthermore, the distinctive levels of temporally and locally regulated 14-3-3γ expression in various brain disorders suggest that it could play a substantial role in brain plasticity of the diseased states. In this review, we introduce the various brain disorders reported to be involved with 14-3-3γ, and summarize the changes of 14-3-3γ expression in each brain disease. We also discuss the potential of 14-3-3γ for treatment and the importance of research on specific 14-3-3 isotypes for an effective therapeutic approach.

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In-vivo administration of clozapine affects behaviour but does not reverse dendritic spine deficits in the 14-3-3ζ KO mouse model of schizophrenia-like disorders

Cited by 14 publications

References 65 publications

14-3-3 Proteins in Glutamatergic Synapses

14-3-3 Proteins in Glutamatergic Synapses

14-3-3 Proteins in Brain Development: Neurogenesis, Neuronal Migration and Neuromorphogenesis

Emerging roles of 14-3-3γ in the brain disorder

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