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Auteur Yusuke ONAKA |
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Improvement by methylphenidate and atomoxetine of social interaction deficits and recognition memory impairment in a mouse model of valproic acid-induced autism / Yuta HARA in Autism Research, 9-9 (September 2016)
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Titre : Improvement by methylphenidate and atomoxetine of social interaction deficits and recognition memory impairment in a mouse model of valproic acid-induced autism Type de document : Texte imprimé et/ou numérique Auteurs : Yuta HARA, Auteur ; Yukio AGO, Auteur ; Atsuki TARUTA, Auteur ; Keisuke KATASHIBA, Auteur ; Shigeru HASEBE, Auteur ; Erika TAKANO, Auteur ; Yusuke ONAKA, Auteur ; Hitoshi HASHIMOTO, Auteur ; Toshio MATSUDA, Auteur ; Kazuhiro TAKUMA, Auteur Article en page(s) : p.926-939 Langues : Anglais (eng) Mots-clés : valproic acid methylphenidate atomoxetine behavioral analysis animal model Index. décimale : PER Périodiques Résumé : Rodents exposed prenatally to valproic acid (VPA) show autism-related behavioral abnormalities. We recently found that prenatal VPA exposure causes a reduction of dopaminergic activity in the prefrontal cortex of male, but not female, mice. This suggests that reduced prefrontal dopaminergic activity is associated with behavioral abnormalities in VPA-treated mice. In the present study, we examined whether the attention deficit/hyperactivity disorder drugs methylphenidate and atomoxetine (which increase dopamine release in the prefrontal cortex, but not striatum, in mice) could alleviate the behavioral abnormalities and changes in dendritic spine morphology induced by prenatal VPA exposure. We found that methylphenidate and atomoxetine increased prefrontal dopamine and noradrenaline release in VPA-treated mice. Acute treatment with methylphenidate or atomoxetine did not alleviate the social interaction deficits or recognition memory impairment in VPA-treated mice, while chronic treatment for 2 weeks did. Methylphenidate or atomoxetine for 2 weeks also improved the prenatal VPA-induced decrease in dendritic spine density in the prefrontal cortex. The effects of these drugs on behaviors and dendritic spine morphology were antagonized by concomitant treatment with the dopamine-D1 receptor antagonist SCH39166 or the dopamine-D2 receptor antagonist raclopride, but not by the ?2-adrenoceptor antagonist idazoxan. These findings suggest that chronic treatment with methylphenidate or atomoxetine improves abnormal behaviors and diminishes the reduction in spine density in VPA-treated mice via a prefrontal dopaminergic system-dependent mechanism. En ligne : http://dx.doi.org/10.1002/aur.1596 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=294
in Autism Research > 9-9 (September 2016) . - p.926-939[article] Improvement by methylphenidate and atomoxetine of social interaction deficits and recognition memory impairment in a mouse model of valproic acid-induced autism [Texte imprimé et/ou numérique] / Yuta HARA, Auteur ; Yukio AGO, Auteur ; Atsuki TARUTA, Auteur ; Keisuke KATASHIBA, Auteur ; Shigeru HASEBE, Auteur ; Erika TAKANO, Auteur ; Yusuke ONAKA, Auteur ; Hitoshi HASHIMOTO, Auteur ; Toshio MATSUDA, Auteur ; Kazuhiro TAKUMA, Auteur . - p.926-939.
Langues : Anglais (eng)
in Autism Research > 9-9 (September 2016) . - p.926-939
Mots-clés : valproic acid methylphenidate atomoxetine behavioral analysis animal model Index. décimale : PER Périodiques Résumé : Rodents exposed prenatally to valproic acid (VPA) show autism-related behavioral abnormalities. We recently found that prenatal VPA exposure causes a reduction of dopaminergic activity in the prefrontal cortex of male, but not female, mice. This suggests that reduced prefrontal dopaminergic activity is associated with behavioral abnormalities in VPA-treated mice. In the present study, we examined whether the attention deficit/hyperactivity disorder drugs methylphenidate and atomoxetine (which increase dopamine release in the prefrontal cortex, but not striatum, in mice) could alleviate the behavioral abnormalities and changes in dendritic spine morphology induced by prenatal VPA exposure. We found that methylphenidate and atomoxetine increased prefrontal dopamine and noradrenaline release in VPA-treated mice. Acute treatment with methylphenidate or atomoxetine did not alleviate the social interaction deficits or recognition memory impairment in VPA-treated mice, while chronic treatment for 2 weeks did. Methylphenidate or atomoxetine for 2 weeks also improved the prenatal VPA-induced decrease in dendritic spine density in the prefrontal cortex. The effects of these drugs on behaviors and dendritic spine morphology were antagonized by concomitant treatment with the dopamine-D1 receptor antagonist SCH39166 or the dopamine-D2 receptor antagonist raclopride, but not by the ?2-adrenoceptor antagonist idazoxan. These findings suggest that chronic treatment with methylphenidate or atomoxetine improves abnormal behaviors and diminishes the reduction in spine density in VPA-treated mice via a prefrontal dopaminergic system-dependent mechanism. En ligne : http://dx.doi.org/10.1002/aur.1596 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=294