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Aripiprazole inhibits polyI:C-induced microglial activation possibly via TRPM7.

Abstract：

:Viral infections during fetal and adolescent periods, as well as during the course of schizophrenia itself have been linked to the onset and/or relapse of a psychosis. We previously reported that the unique antipsychotic aripiprazole, a partial D2 agonist, inhibits the release of tumor necrosis factor (TNF)-α from interferon-γ-activated rodent microglial cells. Polyinosinic-polycytidylic acid (polyI:C) has recently been used as a standard model of viral infections, and recent in vitro studies have shown that microglia are activated by polyI:C. Aripiprazole has been reported to ameliorate behavioral abnormalities in polyI:C-induced mice. To clarify the anti-inflammatory properties of aripiprazole, we investigated the effects of aripiprazole on polyI:C-induced microglial activation in a cellular model of murine microglial cells and possible surrogate cells for human microglia. PolyI:C treatment of murine microglial cells activated the production of TNF-α and enhanced the p38 mitogen-activated protein kinase (MAPK) pathway, whereas aripiprazole inhibited these responses. In addition, polyI:C treatment of possible surrogate cells for human microglia markedly increased TNF-α mRNA expression in cells from three healthy volunteers. Aripiprazole inhibited this increase in cells from two individuals. PolyI:C consistently increased intracellular Ca2+ concentration ([Ca2+]i) in murine microglial cells by influx of extracellular Ca2+. We demonstrated that transient receptor potential in melastatin 7 (TRPM7) channels contributed to this polyI:C-induced increase in [Ca2+]i. Taken together, these data suggest that aripiprazole may be therapeutic for schizophrenia by reducing microglial inflammatory reactions, and TRPM7 may be a novel therapeutic target for schizophrenia. Further studies are needed to validate these findings.

journal_name

Schizophr Res

journal_title

Schizophrenia research

authors

Sato-Kasai M,Kato TA,Ohgidani M,Mizoguchi Y,Sagata N,Inamine S,Horikawa H,Hayakawa K,Shimokawa N,Kyuragi S,Seki Y,Monji A,Kanba S

doi

10.1016/j.schres.2016.08.022

subject

Has Abstract

pub_date

2016-12-01 00:00:00

pages

35-43

issue

1-3

eissn

0920-9964

issn

1573-2509

pii

S0920-9964(16)30372-3

journal_volume

178

pub_type

杂志文章

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