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Neurodevelopmental Disorders

開催日 2014/9/12
時間 14:00 - 15:00
会場 Poster / Exhibition(Event Hall B)

Effects of D-cycloserine on the behavioral impairment in mice induced by prenatal nicotine exposure

  • P2-362
  • 榊原 奈美 / Nami Sakakibara:1 青山 雄紀 / Yuki Aoyama:1,2 宋 由香 / Yuka Soh:1 吉田 あや / Aya Yoshida:1 間宮 隆吉 / Takayoshi Mamiya:1,4 鍋島 俊隆 / Toshitaka Nabeshima:3,4 平松 正行 / Masayuki Hiramatsu:1,4 
  • 1:名城大学薬学部薬品作用学研究室 / Department of Chemical Pharmacology, Faculty of Pharmacy, Meijo University, Nagoya, Japan 2:名古屋大学大学院医学系研究科医療薬学 / Department of Neuropsychopharmacology, Nagoya University Graduate School of Medicine, Nagoya, Japan 3:名城大学薬学部地域医療薬局学 / Department of Regional Pharmaceutical Care and Sciences, Faculty of Pharmacy, Meijo University, Nagoya, Japan 4:特定非営利活動法人 医薬品適正使用推進機構 / Japanese Drug Organization of Appropriate Use and Research, Nagoya, Japan 

It is well known that smoking during pregnancy impairs cognitive and emotional functions in offspring. Previously, we have demonstrated that prenatal nicotine exposure (PNE) during embryonic day 14 to postnatal day 0 (E14–P0) induces the severe behavioral impairment and the reduction of the density of glutamatergic neurons in the prefrontal cortex of mice at the age of 8–12 weeks. In this study, we investigated the behavioral impairment of mice induced by PNE and examined the effects of D–cycloserine (DCS) on the behavioral impairment.
Mice at the age of 8 week were subjected to the elevated plus maze, object based attention, marble burying, and fear conditioning tasks. We found that PNE induced anxiogenic and attention deficits, and reduced the glutamate contents in the prefrontal cortex of PNE–treated mice compared to the sucrose–treated mice.
Systemic treatment (30 mg/kg s.c.) or microinjection (5 nmol/0.5 µL, both sides of the prefrontal cortex, 15° angle from A:+1.7mm, L:±1.0mm from bregma, V:-1.5 mm from the dura) of DCS attenuated behavioral impairment.
These results suggest that (1) PNE may produce the attentional and emotional deficits in mice with hypofunction of glutamatergic system in the prefrontal cortex, and (2) the activation of NMDA receptor may be useful for the treatment of behavioral impairment induced by PNE.

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