Embryonic exposure to valproic acid and neonicotinoid deteriorates the hyperpolarizing GABA shift and impairs long-term potentiation of excitatory transmission in the local circuit of intermediate medial mesopallium of chick telencephalon

Matsushima, Toshiya; Toji, Noriyuki; Wada, Kazuhiro; Shikanai, Hiroki; Izumi, Takeshi

Embryonic exposure to valproic acid and neonicotinoid deteriorates the hyperpolarizing GABA shift and impairs long-term potentiation of excitatory transmission in the local circuit of intermediate medial mesopallium of chick telencephalon

Matsushima, Toshiya; Toji, Noriyuki; Wada, Kazuhiro et al.

Cerebral Cortex, 2025, 35(2), bhaf044

Permalink : https://hdl.handle.net/2115/97429

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論文情報

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アクセス権	open access
URI	https://hdl.handle.net/2115/97429
タイトル	Embryonic exposure to valproic acid and neonicotinoid deteriorates the hyperpolarizing GABA shift and impairs long-term potentiation of excitatory transmission in the local circuit of intermediate medial mesopallium of chick telencephalon
著者	Matsushima, Toshiya ; Toji, Noriyuki ; Wada, Kazuhiro ; Shikanai, Hiroki ; Izumi, Takeshi
e-Rad_Researcher 40190459 著者名 Matsushima, Toshiya
e-Rad_Researcher 20866371 著者名 Toji, Noriyuki
e-Rad_Researcher 70451408 著者名 Wada, Kazuhiro
著者名 Shikanai, Hiroki
e-Rad_Researcher 60312360 著者名 Izumi, Takeshi
言語	英語
キーワード	autism spectrum disorder
	hyperpolarizing GABA shift
	long-term potentiation
	neonicotinoid
	valproic acid
発行日	2025-03-02
出版者	Oxford University Press
収録物名	Cerebral Cortex
巻(号)	35(2)
ページ	bhaf044
抄録	Embryonic exposure to valproic acid and imidacloprid (a neonicotinoid insecticide) impairs filial imprinting in hatchlings, and the deteriorating effects of valproic acid are mitigated by post-hatch injection of bumetanide, a blocker of the chloride intruder Na-K-2Cl cotransporter 1. Here, we report that these exposures depolarized the reversal potential of local GABAergic transmission in the neurons of the intermediate medial mesopallium, the pallial region critical for imprinting. Furthermore, exposure increased field excitatory post-synaptic potentials in pre-tetanus recordings and impaired long-term potentiation (LTP) by low-frequency tetanic stimulation. Bath-applied bumetanide rescued the impaired LTP in the valproic acid slices, whereas VU0463271, a blocker of the chloride extruder KCC2, suppressed LTP in the control slices, suggesting that hyperpolarizing GABA action is necessary for the potentiation of excitatory synaptic transmission. Whereas a steep increase in the gene expression of KCC2 appeared compared to NKCC1 during the peri-hatch development, significant differences were not found between valproic acid and control post-hatch chicks in these genes. Instead, both valproic acid and imidacloprid downregulated several transcriptional regulators (FOS, NR4A1, and NR4A2) and upregulated the RNA component of signal recognition particles (RN7SL1). Despite different chemical actions, valproic acid and imidacloprid could cause common neuronal effects that lead to impaired imprinting.
資源タイプ	学術雑誌論文
出版タイプ	Accepted Manuscript
権利情報	This is a pre-copyedited, author-produced version of an article accepted for publication in Cerebral Cortex following peer review. The version of record Risa Toshiya Matsushima, Noriyuki Toji, Kazuhiro Wada, Hiroki Shikanai, and Takeshi Izumi, Embryonic exposure to valproic acid and neonicotinoid deteriorates the hyperpolarizing GABA shift and impairs long-term potentiation of excitatory transmission in the local circuit of intermediate medial mesopallium of chick telencephalon, Cerebral Cortex, Volume 35, Issue 2, February 2025, bhaf044 is available online at: https://doi.org/10.1093/cercor/bhaf044.
PISSN	1047-3211
EISSN	1460-2199
関連情報 (isVersionOf)	出版社版DOI https://doi.org/10.1093/cercor/bhaf044