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Risperidone and aripiprazole alleviate prenatal valproic acid-induced abnormalities in behaviors and dendritic spine density in mice.

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Title: Risperidone and aripiprazole alleviate prenatal valproic acid-induced abnormalities in behaviors and dendritic spine density in mice.
Authors: Hara, Yuta, Ago, Yukio, Taruta, Atsuki, Hasebe, Shigeru, Kawase, Haruki, Tanabe, Wataru, Tsukada, Shinji, Nakazawa, Takanobu, Hashimoto, Hitoshi, Matsuda, Toshio, Takuma, Kazuhiro
Source: Psychopharmacology. Nov2017, Vol. 234 Issue 21, p3217-3228. 12p.
Subjects: Risperidone, Aripiprazole, Physiological effects of antipsychotic drugs, Valproic acid, Dendritic spines, Mice behavior, Autism spectrum disorders, Dopamine
Abstract: Rationale: Rodents exposed prenatally to valproic acid (VPA) exhibit autism spectrum disorder (ASD)-like behavioral abnormalities. We recently found that prenatal VPA exposure causes hypofunction of the prefrontal dopaminergic system in mice. This suggests that the dopaminergic system may be a potential pharmacological target for treatment of behavioral abnormalities in ASD patients. Objectives: In the present study, we examined the effects of antipsychotic drugs, which affect the dopaminergic system, on the social interaction deficits, recognition memory impairment, and reduction in dendritic spine density in the VPA mouse model of ASD. Results: Both acute and chronic administrations of the atypical antipsychotic drugs risperidone and aripiprazole increased prefrontal dopamine (DA) release, while the typical antipsychotic drug haloperidol did not. Chronic risperidone and aripiprazole, but not haloperidol, increased the expression of c-Fos in the prefrontal cortex, although they all increased c-Fos expression in the striatum. Chronic, but not acute, administrations of risperidone and aripiprazole improved the VPA-induced social interaction deficits and recognition memory impairment, as well as the reduction in dendritic spine density in the prefrontal cortex and hippocampus. In contrast, chronic administration of haloperidol did not ameliorate VPA-induced abnormalities in behaviors and dendritic spine density. Conclusions: These findings indicate that chronic risperidone and aripiprazole treatments improve VPA-induced abnormalities in behaviors and prefrontal dendritic spine density, which may be mediated by repeated elevation of extracellular DA in the prefrontal cortex. Our results also imply that loss of prefrontal dendritic spines may be involved in the abnormal behaviors in the VPA mouse model of ASD. [ABSTRACT FROM AUTHOR]
Copyright of Psychopharmacology is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
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  Data: Risperidone and aripiprazole alleviate prenatal valproic acid-induced abnormalities in behaviors and dendritic spine density in mice.
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  Data: <searchLink fieldCode="AR" term="%22Hara%2C+Yuta%22">Hara, Yuta</searchLink><br /><searchLink fieldCode="AR" term="%22Ago%2C+Yukio%22">Ago, Yukio</searchLink><br /><searchLink fieldCode="AR" term="%22Taruta%2C+Atsuki%22">Taruta, Atsuki</searchLink><br /><searchLink fieldCode="AR" term="%22Hasebe%2C+Shigeru%22">Hasebe, Shigeru</searchLink><br /><searchLink fieldCode="AR" term="%22Kawase%2C+Haruki%22">Kawase, Haruki</searchLink><br /><searchLink fieldCode="AR" term="%22Tanabe%2C+Wataru%22">Tanabe, Wataru</searchLink><br /><searchLink fieldCode="AR" term="%22Tsukada%2C+Shinji%22">Tsukada, Shinji</searchLink><br /><searchLink fieldCode="AR" term="%22Nakazawa%2C+Takanobu%22">Nakazawa, Takanobu</searchLink><br /><searchLink fieldCode="AR" term="%22Hashimoto%2C+Hitoshi%22">Hashimoto, Hitoshi</searchLink><br /><searchLink fieldCode="AR" term="%22Matsuda%2C+Toshio%22">Matsuda, Toshio</searchLink><br /><searchLink fieldCode="AR" term="%22Takuma%2C+Kazuhiro%22">Takuma, Kazuhiro</searchLink>
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  Data: Rationale: Rodents exposed prenatally to valproic acid (VPA) exhibit autism spectrum disorder (ASD)-like behavioral abnormalities. We recently found that prenatal VPA exposure causes hypofunction of the prefrontal dopaminergic system in mice. This suggests that the dopaminergic system may be a potential pharmacological target for treatment of behavioral abnormalities in ASD patients. Objectives: In the present study, we examined the effects of antipsychotic drugs, which affect the dopaminergic system, on the social interaction deficits, recognition memory impairment, and reduction in dendritic spine density in the VPA mouse model of ASD. Results: Both acute and chronic administrations of the atypical antipsychotic drugs risperidone and aripiprazole increased prefrontal dopamine (DA) release, while the typical antipsychotic drug haloperidol did not. Chronic risperidone and aripiprazole, but not haloperidol, increased the expression of c-Fos in the prefrontal cortex, although they all increased c-Fos expression in the striatum. Chronic, but not acute, administrations of risperidone and aripiprazole improved the VPA-induced social interaction deficits and recognition memory impairment, as well as the reduction in dendritic spine density in the prefrontal cortex and hippocampus. In contrast, chronic administration of haloperidol did not ameliorate VPA-induced abnormalities in behaviors and dendritic spine density. Conclusions: These findings indicate that chronic risperidone and aripiprazole treatments improve VPA-induced abnormalities in behaviors and prefrontal dendritic spine density, which may be mediated by repeated elevation of extracellular DA in the prefrontal cortex. Our results also imply that loss of prefrontal dendritic spines may be involved in the abnormal behaviors in the VPA mouse model of ASD. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of Psychopharmacology is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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