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Toll-like receptor-2 deficiency induces schizophrenia-like behaviors in mice
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Toll-like receptor-2 deficiency induces schizophrenia-like behaviors in mice
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Toll-like receptor-2 deficiency induces schizophrenia-like behaviors in mice
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Journal Article
Toll-like receptor-2 deficiency induces schizophrenia-like behaviors in mice
2015
Overview
Dysregulation of the immune system contributes to the pathogenesis of neuropsychiatric disorders including schizophrenia. Here, we demonstrated that toll-like receptor (TLR)-2, a family of pattern-recognition receptors, is involved in the pathogenesis of schizophrenia-like symptoms. Psychotic symptoms such as hyperlocomotion, anxiolytic-like behaviors, prepulse inhibition deficits, social withdrawal and cognitive impairments were observed in TLR-2 knock-out (KO) mice. Ventricle enlargement, a hallmark of schizophrenia, was also observed in TLR-2 KO mouse brains. Levels of p-Akt and p-GSK-3α/β were markedly higher in the brain of TLR-2 KO than wild-type (WT) mice. Antipsychotic drugs such as haloperidol or clozapine reversed behavioral and biochemical alterations in TLR-2 KO mice. Furthermore, p-Akt and p-GSK-3α/β were decreased by treatment with a TLR-2 ligand, lipoteichoic acid, in WT mice. Thus, our data suggest that the dysregulation of the innate immune system by a
TLR-2
deficiency may contribute to the development and/or pathophysiology of schizophrenia-like behaviors via Akt-GSK-3α/β signaling.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ 13/51
/ 13/95
/ 45/29
/ 59/57
/ 64/110
/ 64/60
/ 9/30
/ Animals
/ Antipsychotic Agents - administration & dosage
/ Antipsychotic Agents - pharmacology
/ Anxiety
/ Cerebral Ventricles - pathology
/ Cognition Disorders - genetics
/ Glycogen Synthase Kinase 3 - metabolism
/ Humanities and Social Sciences
/ Mice
/ Proto-Oncogene Proteins c-akt - metabolism
/ Rodents
/ Schizophrenia - drug therapy
/ Science
/ Toll-Like Receptor 2 - deficiency
/ Toll-Like Receptor 2 - genetics
