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Neurodevelopmental Disorders

開催日 2014/9/12
時間 11:00 - 12:00
会場 Poster / Exhibition(Event Hall B)

Prenatal nicotine exposure impaired the proliferation of the neuronal progenitors

  • P2-363
  • 宋 由香 / Yuka Soh:1 青山 雄紀 / Yuki Aoyama:1,2 榊原 奈美 / Nami Sakakibara:1 吉田 あや / Aya Yoshida:1 鳥海 和也 / Kazuya Toriumi: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 known that the smoking during pregnancy impairs neuronal development and affects cognitive and emotional behaviors in offspring, but the detail mechanism is unclear. Previously, we have demonstrated that prenatal nicotine exposure (PNE) from embryonic day 14 to postnatal day 0 (E14–P0) induces severe behavioral impairment in offspring. In this study, we examined whether PNE affects on the neurogenesis in the frontal cortex of mice by immunohistochemistry.
In PNE–treated group, at E14, migration markers such as Pax6 and Tbr2 in the ventricular zone and subventricular zone did not change. At E16 and E18, the numbers of Tbr2–positive cells decreased, but Pax6–positive cells did not change. Also, in PNE–treated group, at E14 and E16, all cell cycle markers such as PCNA (except for G0 phase), pH3 (M phase) and BrdU (S phase) decreased. At E18, the numbers of BrdU–positive cells decreased but PCNA and pH3 positive cells did not change. On the other hand, there were no differences on the distribution of BrdU–positive cells after the birth. However, the numbers of BrdU–positive cells after the birth decreased. In addition, the numbers of glutamatergic neurons labeled by GLS in the frontal cortex were reduced the adulthood.
These results suggest that PNE might impair the proliferations of the neuronal progenitor cells but not neuronal migration, and lead to the behavioral impairment in the adulthood in mice.

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