Hydrogen sulfide and polysulfides induce GABA/glutamate/d-serine release, facilitate hippocampal LTP, and regulate behavioral hyperactivity

書誌事項

公開日
2023-10-31
資源種別
journal article
権利情報
  • https://creativecommons.org/licenses/by/4.0
  • https://creativecommons.org/licenses/by/4.0
DOI
  • 10.1038/s41598-023-44877-y
公開者
Springer Science and Business Media LLC

説明

<jats:title>Abstract</jats:title><jats:p>Hydrogen sulfide (H<jats:sub>2</jats:sub>S) and polysulfides (H<jats:sub>2</jats:sub>S<jats:sub>n</jats:sub>, n ≥ 2) are signaling molecules produced by 3-mercaptopyruvate sulfurtransferase (3MST) that play various physiological roles, including the induction of hippocampal long-term potentiation (LTP), a synaptic model of memory formation, by enhancing N-methyl-<jats:sc>d</jats:sc>-aspartate (NMDA) receptor activity. However, the presynaptic action of H<jats:sub>2</jats:sub>S/H<jats:sub>2</jats:sub>S<jats:sub>n</jats:sub> on neurotransmitter release, regulation of LTP induction, and animal behavior are poorly understood. Here, we showed that H<jats:sub>2</jats:sub>S/H<jats:sub>2</jats:sub>S<jats:sub>2</jats:sub> applied to the rat hippocampus by in vivo microdialysis induces the release of GABA, glutamate, and <jats:sc>d</jats:sc>-serine, a co-agonist of NMDA receptors. Animals with genetically knocked-out 3MST and the target of H<jats:sub>2</jats:sub>S<jats:sub>2</jats:sub>, transient receptor potential ankyrin 1 (TRPA1) channels, revealed that H<jats:sub>2</jats:sub>S/H<jats:sub>2</jats:sub>S<jats:sub>2</jats:sub>, 3MST, and TRPA1 activation play a critical role in LTP induction, and the lack of 3MST causes behavioral hypersensitivity to NMDA receptor antagonism, as in schizophrenia. H<jats:sub>2</jats:sub>S/H<jats:sub>2</jats:sub>S<jats:sub>n</jats:sub>, 3MST, and TRPA1 channels have therapeutic potential for psychiatric diseases and cognitive deficits.</jats:p>

収録刊行物

  • Scientific Reports

    Scientific Reports 13 (1), 17663-, 2023-10-31

    Springer Science and Business Media LLC

被引用文献 (2)*注記

もっと見る

参考文献 (69)*注記

もっと見る

関連プロジェクト

もっと見る

詳細情報 詳細情報について

問題の指摘

ページトップへ