Ban-yu Saitoh

Dr. Ban-yu Saitoh

orcid

Research Focus & Metrics

Academic Career Length

11Years (2016-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 May 2016 in Journal of the Neurological Sciences
Verified
Journal Article
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BSBan-yu Saitoh
Ban-yu Saitoh
SHShintaro Hayashi
Shintaro Hayashi
KOKatsuya Ogata
Katsuya Ogata
TUTaira Uehara
Taira Uehara
HDHikaru Doi
Hikaru Doi
JKJun-ichi Kira
Jun-ichi Kira

Verified
Journal Article
Open access
PDF file
ETEizo Tanaka
Eizo Tanaka
RYRyo Yamasaki
Ryo Yamasaki
BSBan-yu Saitoh
Ban-yu Saitoh
AAAmina Ahmed Abdelhadi
Amina Ahmed Abdelhadi
SNSatoshi Nagata
Satoshi Nagata
NINoriko Isobe
Noriko Isobe
Autism spectrum disorder (ASD) is one of the most prevalent neurodevelopmental disorders. To explore its pathophysiology, we investigated the association between neonatal allergic exposure and behavioral changes. Adult female C57BL/6J mice were immunized with adjuvant (aluminum hydroxide) or ovalbumin emulsified with adjuvant. After immunization, the mice were mated, and offspring were born at full term. The postnatal dams and infants were then simultaneously exposed to an allergen (ovalbumin) or vehicle via inhalation. After weaning, behavioral testing and histopathological analyses were conducted on male offspring. Compared with the vehicle-exposed offspring, the ovalbumin-exposed offspring had decreased sociability and increased repetitive behavior, thus representing an ASD-like phenotype in mice. Moreover, histopathological analyses revealed that the ovalbumin-exposed mice had increased astroglial, microglial, and eosinophilic infiltration in the olfactory bulb, as well as increased eosinophils in the nasal mucosa. The ovalbumin-exposed mice also had decreased dendritic spine density and a lower proportion of mature spines, suggesting the impairment of stimulus-induced synaptogenesis. In conclusion, postnatal allergic exposure induced an ASD-like phenotype, as well as allergic rhinitis, which was followed by glial inflammation in the olfactory bulb parenchyma.