TY  - JOUR
  - Desbonnet, L,O'Tuathaigh, C,Clarke, G,O'Leary, C,Petit, E,Clarke, N,Tighe, O,Lai, D,Harvey, R,Cryan, JF,Dinan, TG,Waddington, JL
  - 2012
  - January
  - Brain Behav Immun
  - Phenotypic effects of repeated psychosocial stress during adolescence in mice mutant for the schizophrenia risk gene neuregulin-1: A putative model of gene x environment interaction
  - Validated
  - ()
  - Social defeat stress Neuregulin 1 Behavioural phenotype Working memory Prepulse inhibition Cytokines Concanavalin A Lipopolysaccharide Gene x environment interaction Schizophrenia REPEATED SOCIAL DEFEAT PREPULSE INHIBITION NEUROTROPHIC FACTOR SIGNALING PATHWAYS PREFRONTAL CORTEX KNOCKOUT MICE ANIMAL-MODELS BASE-LINE BRAIN DEPRESSION
  - 26
  - 660
  - 671
  - There is a paucity of animal models by which the contributions of environmental and genetic factors to the pathobiology of psychosis can be investigated. This study examined the individual and combined effects of chronic social stress during adolescence and deletion of the schizophrenia risk gene neuregulin-1 (NRG1) on adult mouse phenotype. Mice were exposed to repeated social defeat stress during adolescence and assessed for exploratory behaviour, working memory, sucrose preference, social behaviour and prepulse inhibition in adulthood. Thereafter, in vitro cytokine responses to mitogen stimulation and corticosterone inhibition were assayed in spleen cells, with measurement of cytokine and brain-derived neurotrophic factor (BDNF) mRNA in frontal cortex, hippocampus and striatum. NRG1 mutants exhibited hyperactivity, decreased anxiety, impaired sensorimotor gating and reduced preference for social novelty. The effects of stress on exploratory/anxiety-related parameters, spatial working memory, sucrose preference and basal cytokine levels were modified by NRG1 deletion. Stress also exerted varied effect on spleen cytokine response to concanavalin A and brain cytokine and BDNF mRNA expression in NRG1 mutants. The experience of psychosocial stress during adolescence may trigger further pathobiological features that contribute to the development of schizophrenia, particularly in those with underlying NRG1 gene abnormalities. This model elaborates the importance of gene x environment interactions in the etiology of schizophrenia. (C) 2012 Elsevier Inc. All rights reserved.
  - DOI 10.1016/j.bbi.2012.02.010
DA  - 2012/01
ER  - 

@article{V146554400,
   = {Desbonnet,  L and O'Tuathaigh,  C and Clarke,  G and O'Leary,  C and Petit,  E and Clarke,  N and Tighe,  O and Lai,  D and Harvey,  R and Cryan,  JF and Dinan,  TG and Waddington,  JL },
   = {2012},
   = {January},
   = {Brain Behav Immun},
   = {Phenotypic effects of repeated psychosocial stress during adolescence in mice mutant for the schizophrenia risk gene neuregulin-1: A putative model of gene x environment interaction},
   = {Validated},
   = {()},
   = {Social defeat stress Neuregulin 1 Behavioural phenotype Working memory Prepulse inhibition Cytokines Concanavalin A Lipopolysaccharide Gene x environment interaction Schizophrenia REPEATED SOCIAL DEFEAT PREPULSE INHIBITION NEUROTROPHIC FACTOR SIGNALING PATHWAYS PREFRONTAL CORTEX KNOCKOUT MICE ANIMAL-MODELS BASE-LINE BRAIN DEPRESSION},
   = {26},
  pages = {660--671},
   = {{There is a paucity of animal models by which the contributions of environmental and genetic factors to the pathobiology of psychosis can be investigated. This study examined the individual and combined effects of chronic social stress during adolescence and deletion of the schizophrenia risk gene neuregulin-1 (NRG1) on adult mouse phenotype. Mice were exposed to repeated social defeat stress during adolescence and assessed for exploratory behaviour, working memory, sucrose preference, social behaviour and prepulse inhibition in adulthood. Thereafter, in vitro cytokine responses to mitogen stimulation and corticosterone inhibition were assayed in spleen cells, with measurement of cytokine and brain-derived neurotrophic factor (BDNF) mRNA in frontal cortex, hippocampus and striatum. NRG1 mutants exhibited hyperactivity, decreased anxiety, impaired sensorimotor gating and reduced preference for social novelty. The effects of stress on exploratory/anxiety-related parameters, spatial working memory, sucrose preference and basal cytokine levels were modified by NRG1 deletion. Stress also exerted varied effect on spleen cytokine response to concanavalin A and brain cytokine and BDNF mRNA expression in NRG1 mutants. The experience of psychosocial stress during adolescence may trigger further pathobiological features that contribute to the development of schizophrenia, particularly in those with underlying NRG1 gene abnormalities. This model elaborates the importance of gene x environment interactions in the etiology of schizophrenia. (C) 2012 Elsevier Inc. All rights reserved.}},
   = {DOI 10.1016/j.bbi.2012.02.010},
  source = {IRIS}
}