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Exp Ther Med. 2018 Jan;15(1):745-750. doi: 10.3892/etm.2017.5443. Epub 2017 Nov 6.

Aripiprazole exerts a neuroprotective effect in mouse focal cerebral ischemia.

Gil CH1,2, Kim YR1,3, Lee HJ1,2, Jung DH1,2, Shin HK1,2,3,4, Choi BT1,2,3,4.

Author information

1
Department of Korean Medical Science, School of Korean Medicine, Pusan National University, Yangsan, Gyeongsangnam 50612, Republic of Korea.
2
Graduate Training Program of Korean Medicine for Healthy Aging, School of Korean Medicine, Pusan National University, Yangsan, Gyeongsangnam 50612, Republic of Korea.
3
Korean Medical Science Research Center for Healthy-Aging, School of Korean Medicine, Pusan National University, Yangsan, Gyeongsangnam 50612, Republic of Korea.
4
Division of Meridian and Structural Medicine, School of Korean Medicine, Pusan National University, Yangsan, Gyeongsangnam 50612, Republic of Korea.

Abstract

Previous studies have demonstrated that aripiprazole (APZ), a third-generation atypical antipsychotic drug, exhibits anti-depressant and neuroprotective effects by promoting dopaminergic neuronal cell recovery in stroke. To investigate the neuroprotective effects of APZ, behavioral and histopathological experiments were performed in the current study a mouse model of middle cerebral artery occlusion (MCAO)-induced ischemia following administration of APZ. The subacute phase of ischemic assaults was divided into 3 periods, each with a duration of 5 days, according to the start of APZ (3 mg/kg) administration (1-5, 5-9 or 10-14 days following MCAO). The beneficial effects of APZ on motor behavior demonstrated in the cylinder, rotarod and wire suspension tests were greatest when APZ was administered 1-5 days following MCAO, with clear improvements in motor function compared with vehicle-treated mice. Histopathological analysis revealed that prominent atrophic changes occurred in the striatum of MCAO mice and that these changes were reduced following APZ treatment. APZ also attenuated dopaminergic neuronal injury in the striatum. Cell death and microglial activation were decreased and the expression of Ca2+/calmodulin-dependent protein kinase II δ was enhanced following APZ treatment. These results indicate that the atypical antipsychotic drug, APZ, exhibits a neuroprotective effect in dopaminergic neuronal cells that may improve behavioral function following ischemic stroke.

KEYWORDS:

aripiprazole; cell death; ischemic stroke; microglia; neuroprotection

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