{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T16:15:59Z","timestamp":1788365759735,"version":"build-2803163510"},"reference-count":75,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2026,1,29]],"date-time":"2026-01-29T00:00:00Z","timestamp":1769644800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,1,29]],"date-time":"2026-01-29T00:00:00Z","timestamp":1769644800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Environmental Toxicology"],"published-print":{"date-parts":[[2026,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Maternal exposure to imidacloprid (IMI) suppresses hippocampal neurogenesis in rat offspring. This study investigated the antioxidant effects of an amorphous formula of curcumin (CUR) given at a supplement level on IMI\u2010induced suppression of neurogenesis to clarify the toxicity mechanisms. Maternal rats were given a diet containing 750\u2010ppm IMI and drinking water with or without 120\u2010ppm CUR from gestational day (GD) 6 until weaning at 21\u2009days post\u2010delivery. Then, offspring received CUR similarly until postnatal day 77 in adulthood. At weaning, IMI had suppressed neurogenesis and synaptic plasticity in granule cells, which may be related to suppressed reelin and parvalbumin signaling of GABAergic interneurons. IMI exposure increased CD68\n                    <jats:sup>+<\/jats:sup>\n                    microglia, decreased CD163\n                    <jats:sup>+<\/jats:sup>\n                    microglia, and upregulated\n                    <jats:italic>Nos2<\/jats:italic>\n                    , suggesting M1 polarization; IMI also downregulated\n                    <jats:italic>Tnf<\/jats:italic>\n                    but did not change the transcript levels of other M1 cytokine genes, suggesting an immunocompromised state. IMI also suppressed hippocampal antioxidant capacity. CUR restored hippocampal antioxidant capacity and ameliorated neurogenesis and synaptic plasticity, involving parvalbumin\n                    <jats:sup>+<\/jats:sup>\n                    interneuron restoration through enhancing NMDAR2D\u2010mediated glutamatergic signaling. The IMI\u2010induced immunocompromised state and oxidative stress\u2010related effects disappeared in adulthood. However, IMI progressively suppressed neurogenesis, possibly associated with suppressed NMDAR2D\u2010mediated glutamatergic signaling. IMI also suppressed VGLUT2\u2010based glutamatergic signaling in granule cells. CUR increased synaptic plasticity in granule cells by enhancing VGLUT2\u2010based glutamatergic signaling and NMDAR2D\u2010mediated glutamatergic signaling. These results suggest that IMI continuously suppresses hippocampal neurogenesis and synaptic plasticity in granule cells into adulthood by increasing susceptibility to oxidative stress during exposure. CUR effectively ameliorated the IMI\u2010induced suppression of neurogenesis at weaning and synaptic plasticity until adulthood.\n                  <\/jats:p>","DOI":"10.1002\/tox.70044","type":"journal-article","created":{"date-parts":[[2026,1,29]],"date-time":"2026-01-29T08:55:52Z","timestamp":1769676952000},"page":"935-956","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Ameliorating Effect of Continuous Treatment With an Amorphous Formula of Curcumin on Maternal Imidacloprid Exposure\u2010Induced Suppression of Hippocampal Neurogenesis in Rats"],"prefix":"10.1002","volume":"41","author":[{"given":"Yuri","family":"Ebizuka","sequence":"first","affiliation":[{"name":"Laboratory of Veterinary Pathology Tokyo University of Agriculture and Technology  Tokyo Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8551-9319","authenticated-orcid":false,"given":"Xinyu","family":"Zou","sequence":"additional","affiliation":[{"name":"Laboratory of Veterinary Pathology Tokyo University of Agriculture and Technology  Tokyo Japan"},{"name":"Cooperative Division of Veterinary Sciences, Graduate School of Agriculture Tokyo University of Agriculture and Technology  Tokyo Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nanami","family":"Watanabe","sequence":"additional","affiliation":[{"name":"Laboratory of Veterinary Pathology Tokyo University of Agriculture and Technology  Tokyo Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mai","family":"Hirata","sequence":"additional","affiliation":[{"name":"Laboratory of Veterinary Pathology Tokyo University of Agriculture and Technology  Tokyo Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Susumu","family":"Yamashita","sequence":"additional","affiliation":[{"name":"Laboratory of Veterinary Pathology Tokyo University of Agriculture and Technology  Tokyo Japan"},{"name":"Medical Evaluation Engineering, Olympus Medical Systems Corporation  Tokyo Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2219-9634","authenticated-orcid":false,"given":"Tetsuhito","family":"Kigata","sequence":"additional","affiliation":[{"name":"Cooperative Division of Veterinary Sciences, Graduate School of Agriculture Tokyo University of Agriculture and Technology  Tokyo Japan"},{"name":"Laboratory of Veterinary Anatomy Tokyo University of Agriculture and Technology  Tokyo Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0001-8369-9798","authenticated-orcid":false,"given":"Qian","family":"Tang","sequence":"additional","affiliation":[{"name":"General Toxicology Department, TriApex Laboratories Co., Ltd.  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