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Investigation of gene effects and epistatic interactions between Akt1 and neuregulin 1 in the regulation of behavioral phenotypes and social functions in genetic mouse models of schizophrenia

Overview of attention for article published in Frontiers in Behavioral Neuroscience, January 2015
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Title
Investigation of gene effects and epistatic interactions between Akt1 and neuregulin 1 in the regulation of behavioral phenotypes and social functions in genetic mouse models of schizophrenia
Published in
Frontiers in Behavioral Neuroscience, January 2015
DOI 10.3389/fnbeh.2014.00455
Pubmed ID
Authors

Ching-Hsun Huang, Ju-Chun Pei, Da-Zhong Luo, Ching Chen, Yi-Wen Chen, Wen-Sung Lai

Abstract

Accumulating evidence from human genetic studies has suggested several functional candidate genes that might contribute to susceptibility to schizophrenia, including AKT1 and neuregulin 1 (NRG1). Recent findings also revealed that NRG1 stimulates the PI3-kinase/AKT signaling pathway, which might be involved in the functional outcomes of some schizophrenic patients. The aim of this study was to evaluate the effect of Akt1-deficiency and Nrg1-deficiency alone or in combination in the regulation of behavioral phenotypes, cognition, and social functions using genetically modified mice as a model. Male Akt1 (+/-), Nrg1 (+/-), and double mutant mice were bred and compared with their wild-type (WT) littermate controls. In Experiment 1, general physical examination revealed that all mutant mice displayed a normal profile of body weight during development and a normal brain activity with microPET scan. In Experiment 2, no significant genotypic differences were found in our basic behavioral phenotyping, including locomotion, anxiety-like behavior, and sensorimotor gating function. However, both Nrg1 (+/-) and double mutant mice exhibited impaired episodic-like memory. Double mutant mice also had impaired sociability. In Experiment 3, a synergistic epistasis between Akt1 and Nrg1 was further confirmed in double mutant mice in that they had impaired social interaction compared to the other 3 groups, especially encountering with a novel male or an ovariectomized female. Double mutant and Nrg1 (+/-) mice also emitted fewer female urine-induced ultrasonic vocalization calls. Collectively, our results indicate that double deficiency of Akt1 and Nrg1 can result in the impairment of social cognitive functions, which might be pertinent to the pathogenesis of schizophrenia-related social cognition.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 37 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United Kingdom 1 3%
Unknown 36 97%

Demographic breakdown

Readers by professional status Count As %
Researcher 9 24%
Student > Ph. D. Student 7 19%
Student > Master 4 11%
Student > Doctoral Student 2 5%
Student > Postgraduate 2 5%
Other 3 8%
Unknown 10 27%
Readers by discipline Count As %
Neuroscience 7 19%
Psychology 6 16%
Agricultural and Biological Sciences 3 8%
Biochemistry, Genetics and Molecular Biology 2 5%
Engineering 2 5%
Other 5 14%
Unknown 12 32%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 18 February 2015.
All research outputs
#20,262,276
of 22,792,160 outputs
Outputs from Frontiers in Behavioral Neuroscience
#2,826
of 3,165 outputs
Outputs of similar age
#297,286
of 353,610 outputs
Outputs of similar age from Frontiers in Behavioral Neuroscience
#60
of 66 outputs
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