イミダクロプリドの発達期曝露により誘発されるラットの海馬神経新生障害に対する非晶質クルクミンの保護効果

海老塚 由理; Xinyu ZOU; Qian TANG; 尾城 椋太; 小澤 俊介; 渡邊 ナナ美; 平田 舞; 滝本 美桜; 中尾 友洋; 小柳 美穂子; 吉田 敏則; 渋谷 淳

doi:10.14869/toxpt.51.1.0_P-30S

The 51st Annual Meeting of the Japanese Society of Toxicology

Session ID : P-30S

DOI https://doi.org/10.14869/toxpt.51.1.0_P-30S

Conference information

Host: The Japanese Society of Toxicology

Name : The 51st Annual Meeting of the Japanese Society of Toxicology

Date : July 03, 2024 - July 05, 2024

Poster Session

Study on the protective effect of amorphous formula of curcumin on maternal imidacloprid exposure-induced disruptive hippocampal neurogenesis in rats

*Yuri EBIZUKA, Xinyu ZOU, Qian TANG, Ryota OJIRO, Shunsuke OZAWA, Nanami WATANABE, Mai HIRATA, Mio TAKIMOTO, Tomohiro NAKAO, Mihoko KOYANAGI, Toshinori YOSHIDA, Makoto SHIBUTANI

Author information

*Yuri EBIZUKA
Laboratory of Veterinary Pathology, Tokyo University of Agriculture and Technology
Xinyu ZOU
Laboratory of Veterinary Pathology, Tokyo University of Agriculture and Technology
Cooperative Division of Veterinary Sciences, Graduate School of Agriculture, Tokyo University of Agriculture and Technology
Qian TANG
Laboratory of Veterinary Pathology, Tokyo University of Agriculture and Technology
Cooperative Division of Veterinary Sciences, Graduate School of Agriculture, Tokyo University of Agriculture and Technology
Ryota OJIRO
Laboratory of Veterinary Pathology, Tokyo University of Agriculture and Technology
Cooperative Division of Veterinary Sciences, Graduate School of Agriculture, Tokyo University of Agriculture and Technology
Shunsuke OZAWA
Laboratory of Veterinary Pathology, Tokyo University of Agriculture and Technology
Cooperative Division of Veterinary Sciences, Graduate School of Agriculture, Tokyo University of Agriculture and Technology
Nanami WATANABE
Laboratory of Veterinary Pathology, Tokyo University of Agriculture and Technology
Mai HIRATA
Laboratory of Veterinary Pathology, Tokyo University of Agriculture and Technology
Mio TAKIMOTO
Laboratory of Veterinary Pathology, Tokyo University of Agriculture and Technology
Tomohiro NAKAO
San-Ei Gen F.F.I., Inc.
Mihoko KOYANAGI
San-Ei Gen F.F.I., Inc.
Toshinori YOSHIDA
Laboratory of Veterinary Pathology, Tokyo University of Agriculture and Technology
Cooperative Division of Veterinary Sciences, Graduate School of Agriculture, Tokyo University of Agriculture and Technology
Makoto SHIBUTANI
Laboratory of Veterinary Pathology, Tokyo University of Agriculture and Technology

CONFERENCE PROCEEDINGS FREE ACCESS

Details

Abstract

Introduction: We previously reported disruptive hippocampal neurogenesis by maternal exposure to neonicotinoid pesticide imidacloprid (IMI) in rats. In this study, we investigated the protective effect of amorphous formula of curcumin (CUR) against IMI-induced disruptive neurogenesis.

Methods: Maternal rats were administered 750 ppm IMI in diet and 120 ppm CUR in drinking water from gestation day 6 to day 21 post-delivery at weaning. After weaning, offspring continued to receive CUR until postnatal day 77 in adulthood.

Results and Discussion: IMI persistently suppressed hippocampal neurogenesis and synaptic plasticity of granule cells until adulthood. IMI decreased the expression of antioxidant enzyme genes on weaning, suggesting increased susceptibility to oxidative stress during the weaning period, whereas no oxidative stress effect was evident in adulthood. These results suggest involvement of suppression of GABAergic interneuron regulation on neurogenesis and synaptic plasticity by increased sensitivity to oxidative stress at weaning. CUR showed sustained interneuron-mediated neuroprotection; however, because CUR did not exert antioxidant effects, CUR may have restored neurogenesis and synaptic plasticity through direct protective effects on interneurons.

Conclusion: IMI persistently suppressed hippocampal neurogenesis and synaptic plasticity of granule cells, involving suppressed interneuron regulation through oxidative stress toxicity at weaning. CUR sustained neuroprotection on neurogenesis and synaptic plasticity through direct protective effects on interneurons.

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