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Peer-reviewedCC BYPLOS One

Paroxetine-induced transient apoptosis with delayed neurogenesis triggers brain-preferential regeneration in developing zebrafish

  • Tomomi Sato1,2
  • Kaito Saito3
  • Tsubasa Oyu3
  • Kazuna Yamaguchi3
  • Maiko Osawa4
  • Yuki Shiko4
  • Yohei Kawasaki4
  • Tomohiro Kurisaki1
  • Sachiko Tsuda3
  • Takeshi Kajihara2
  • Masabumi Nagashima1
4 affiliations
  1. 1Department of Anatomy, School of Medicine, Saitama Medical University, Moroyama-machi, Saitama, Japan.
  2. 2Department of Obstetrics and Gynecology, School of Medicine, Saitama Medical University, Moroyama-machi, Saitama, Japan.
  3. 3Division of Life Science, Graduate School of Science and Engineering, Saitama University, Saitama City, Saitama, Japan.
  4. 4Department of Biostatics, School of Medicine, Saitama Medical University, Moroyama-machi, Saitama, Japan.
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Abstract

Autism spectrum disorder (ASD) is a neurodevelopmental condition caused by a combination of genetic and environmental factors. Its cardinal symptoms include impaired social behavior involving the amygdala. Maternal use of antidepressants such as paroxetine during early pregnancy increases the risk of ASD in offspring. However, the underlying pathogenic mechanisms remain poorly understood. Herein, we demonstrate that early exposure of zebrafish embryos to paroxetine delays neurogenesis in the optic tectum and telencephalon, including a region corresponding to the mammalian amygdala. Paroxetine-treated embryos exhibit growth restriction characterized by small heads and short-body lengths resulting from transient apoptosis. This phenotype resembles the early-onset fetal growth restriction (FGR) associated with ASD. Interestingly, we observed regeneration of delayed neurogenesis in the reduced brain following paroxetine withdrawal. This regenerative process was accompanied by extended retinotectal projections, suggesting brain-preferential regeneration. Finally, we examined the social behavior of paroxetine-treated fish. Taken together, our findings suggest a biological mechanism linking early paroxetine exposure, a risk factor for ASD, to its pathogenesis.

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Cite

BibTeXRIS
BibTeX
@article{sato2026paroxetineinduced,
  title = {{Paroxetine-induced transient apoptosis with delayed neurogenesis triggers brain-preferential regeneration in developing zebrafish}},
  author = {Tomomi Sato and Kaito Saito and Tsubasa Oyu and Kazuna Yamaguchi and Maiko Osawa and Yuki Shiko and Yohei Kawasaki and Tomohiro Kurisaki and Sachiko Tsuda and Takeshi Kajihara and Masabumi Nagashima},
  journal = {PLOS One},
  year = {2026},
  month = oct,
  doi = {10.1371/journal.pone.0345903},
  url = {https://doi.org/10.1371/journal.pone.0345903},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Paroxetine-induced transient apoptosis with delayed neurogenesis triggers brain-preferential regeneration in developing zebrafish
AU  - Tomomi Sato
AU  - Kaito Saito
AU  - Tsubasa Oyu
AU  - Kazuna Yamaguchi
AU  - Maiko Osawa
AU  - Yuki Shiko
AU  - Yohei Kawasaki
AU  - Tomohiro Kurisaki
AU  - Sachiko Tsuda
AU  - Takeshi Kajihara
AU  - Masabumi Nagashima
PY  - 2026
DA  - 2026/10/30
JO  - PLOS One
DO  - 10.1371/journal.pone.0345903
UR  - https://doi.org/10.1371/journal.pone.0345903
AB  - Autism spectrum disorder (ASD) is a neurodevelopmental condition caused by a combination of genetic and environmental factors. Its cardinal symptoms include impaired social behavior involving the amygdala. Maternal use of antidepressants such as paroxetine during early pregnancy increases the risk of ASD in offspring. However, the underlying pathogenic mechanisms remain poorly understood. Herein, we demonstrate that early exposure of zebrafish embryos to paroxetine delays neurogenesis in the optic tectum and telencephalon, including a region corresponding to the mammalian amygdala. Paroxetine-treated embryos exhibit growth restriction characterized by small heads and short-body lengths resulting from transient apoptosis. This phenotype resembles the early-onset fetal growth restriction (FGR) associated with ASD. Interestingly, we observed regeneration of delayed neurogenesis in the reduced brain following paroxetine withdrawal. This regenerative process was accompanied by extended retinotectal projections, suggesting brain-preferential regeneration. Finally, we examined the social behavior of paroxetine-treated fish. Taken together, our findings suggest a biological mechanism linking early paroxetine exposure, a risk factor for ASD, to its pathogenesis.
SN  - 1932-6203
ER  -