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Milnacipran Remediates Impulsive Deficits in Rats with Lesions of the Ventromedial Prefrontal Cortex

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Title: Milnacipran Remediates Impulsive Deficits in Rats with Lesions of the Ventromedial Prefrontal Cortex
Authors: Tsutsui-Kimura, Iku Browse this author
Yoshida, Takayuki Browse this author →KAKEN DB
Ohmura, Yu Browse this author →KAKEN DB
Izumi, Takeshi Browse this author →KAKEN DB
Yoshioka, Mitsuhiro Browse this author →KAKEN DB
Keywords: inhibitory control
infralimbic cortex
spinogenesis
impulsive behavior
BDNF
Issue Date: Mar-2015
Publisher: Oxford University Press
Journal Title: International journal of neuropsychopharmacology
Volume: 18
Issue: 5
Start Page: pyu083
Publisher DOI: 10.1093/ijnp/pyu083
Abstract: Background: Deficits in impulse control are often observed in psychiatric disorders in which abnormalities of the prefrontal cortex are observed, including attention-deficit/hyperactivity disorder and bipolar disorder. We recently found that milnacipran, a serotonin/noradrenaline reuptake inhibitor, could suppress impulsive action in normal rats. However, whether milnacipran could suppress elevated impulsive action in rats with lesions of the ventromedial prefrontal cortex, which is functionally comparable with the human prefrontal cortex, remains unknown. Methods: Selective lesions of the ventromedial prefrontal cortex were made using quinolinic acid in rats previously trained on a 3-choice serial reaction time task. Sham rats received phosphate buffered saline. Following a period of recovery, milnacipran ( 0 or 10 mg/kg/d x 14 days) was orally administered 60 minutes prior to testing on the 3-choice task. After 7 days of drug cessation, Western blotting, immunohistochemistry, electrophysiological analysis, and morphological analysis were conducted. Results: Lesions of the ventromedial prefrontal cortex induced impulsive deficits, and repeated milnacipran ameliorated the impulsive deficit both during the dosing period and after the cessation of the drug. Repeated milnacipran remediated the protein levels of mature brain-derived neurotrophic factor and postsynaptic density-95, dendritic spine density, and excitatory currents in the few surviving neurons in the ventromedial prefrontal cortex of ventromedial prefrontal cortex-lesioned rats. Conclusions: The findings of this study suggest that milnacipran treatment could be a novel strategy for the treatment of psychiatric disorders that are associated with a lack of impulse control.
Rights: http://creativecommons.org/licenses/by-nc/4.0
Type: article
URI: http://hdl.handle.net/2115/59283
Appears in Collections:医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 大村 優

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