Park, Se Jin
Lee, Jee Youn
Kim, Sang Jeong
Choi, Se-Young
Yune, Tae Young
Ryu, Jong Hoon
Article History
Received: 12 October 2014
Accepted: 22 January 2015
First Online: 17 February 2015
Change Date: 18 September 2015
Change Type: Update
Change Details: A correction has been published and is appended to both the HTML and PDF versions of this paper. The error has not been fixed in the paper.
Change Date: 18 September 2015
Change Type: Erratum
Change Details: 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 <i>TLR-2</i> deficiency may contribute to the development and/or pathophysiology of schizophrenia-like behaviors via Akt-GSK-3α/β signaling.
Competing interests
: The authors declare no competing financial interests.