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Neuregulin-1 mutant mice indicate motor and sensory deficits, indeed few references for schizophrenia endophenotype model

Item Type:Article
Title:Neuregulin-1 mutant mice indicate motor and sensory deficits, indeed few references for schizophrenia endophenotype model
Creators Name:Schneider, S. and Götz, K. and Birchmeier, C. and Schwegler, H. and Roskoden, T.
Abstract:Neuregulins (Nrg) are a gene family that binds to tyrosine kinase receptors of the ErbB family. The protein of Nrg1 is to be involved in heart formation, migration of neurons, axonal pathfinding and synaptic function. A relation between Nrg1 and schizophrenia is assumed. Chronic impairment in schizophrenia is characterized by different positive and negative symptoms. Detectable markers of this disease in human and in animal models are activity, social behavior and sensory processing. In this study we compared heterozygous Nrg1 mutant mice in behavior and quantification of dopaminergic and serotoninergic neurons with wild type-like littermates. In the Nrg1 mutant mice the epidermal growth factor-like domain is replaced by the neomycin resistance gene. We found significant differences in locomotor and pain perception behavior. No differences were found in specific schizophrenia social interaction and prepulse inhibition behavior. The number of dopaminergic and serotoninergic neurons did not differ in the investigated regions ventral tegmental area, substantia nigra, periaqueductal grey and raphe nuclei. In conclusion, this analyzed Nrg1 mutant mice model did not serve as a complete schizophrenia model. Particular aspects of schizophrenia disease in locomotor and sensory behavior deficits could represent in this Nrg1 mutant mice. Beside several different models could Nrg1 deficiency represent an endophenotype of schizophrenia disease.
Keywords:Neuregulin, Nrg1, Behavior, Schizophrenia, Dopaminergic, Serotoninergic, Animals, Mice, Transgenic
Source:Behavioural Brain Research
Number:Pt A
Page Range:177-185
Date:30 March 2017
Official Publication:https://doi.org/10.1016/j.bbr.2017.01.022
PubMed:View item in PubMed

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