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Neuroprotection, Neurotoxicity and Neuroinflammation

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

Effects of developmental exposure to diesel engine exhaust origin secondary organic aerosol on social and learning behavior in adult mice

  • P1-341
  • Win-Shwe Tin-Tin:1,2 Fumihiko Maekawa:1 Chaw Kyi-Tha-Thu:2 Yuji Fujitani:1 Rie Yanagisawa:1 Akiko Furuyama:1 Shinji Tsukahara:2 Keiko Nohara:1 Hiroshi Nitta:1 Seishiro Hirano:1 
  • 1:National Institute for Environmental Studies, Tsukuba, Japan 2:Division of Life Science, Graduate School of Science and Engineering, Saitama University, Saitama, Japan 

Background: Secondary organic aerosol (SOA) is a component of PM 2.5 and formed in the atmosphere by oxidation of products from volatile organic compounds. In the present study, we aimed to investigate the effects of developmental exposure to diesel exhaust (DE)-SOA on social and learning behavior in mice.
Methods: We generated the SOA by oxidation of diesel exhaust particle mixed with ozone. Pregnant BALB/c mice were exposed to clean air (control), diesel exhaust (DE), DE-SOA and filtered DE (gas only) in the inhalation chambers for gestational day 13 to postnatal day 21. Social behavior of male offspring at the age of 14 weeks was examined by three chambers social behavioral apparatus with Any-maze software and social behavior-related gene expressions in the hypothalamus by real-time RT-PCR analysis. On the other hand, spatial learning ability and gene expressions related to learning in the prefrontal cortex were examined by automated behavioral analysis system IntelliCage and by real-time RT-PCR analysis, respectively.
Results: Sociability, social novelty preference and social interaction were remarkably impaired and mRNA expressions of estrogen receptor-alpha and oxytocin receptor were significantly decreased in DE-SOA-exposed mice. Increased visit error to the wrong corners was found in the study using IntelliCage. RNA expression of long interspersed nucleotide element-1 (LINE-1), a potential marker for mental disorders, was up-regulated in DE-SOA-exposed mice.
Discussion: These results suggest that the constituent(s) of DE-SOA may trigger late-onset neurotoxicity and affect social behavior and spatial learning based on the impaired gene expressions in the hypothalamus and the prefrontal cortex, respectively.

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