Fluoxetine-induced dematuration of hippocampal neurons and adult cortical neurogenesis in the common marmoset

• 中村, 克樹

  Division of Systems Medical Science, Institute for Comprehensive Medical Science, Fujita Health University･Laboratory of Nutritional Brain Science, Department of Food Science and Nutrition, Mukogawa Women’s University

• Hagihara, Hideo

  Division of Systems Medical Science, Institute for Comprehensive Medical Science, Fujita Health University

• Miwa, Miki

  Cognitive Neuroscience Section, Primate Research Institute, Kyoto University

• Nakamura, Katsuki

  Cognitive Neuroscience Section, Primate Research Institute, Kyoto University

• Miyakawa, Tsuyoshi

  Division of Systems Medical Science, Institute for Comprehensive Medical Science, Fujita Health University

抄録

The selective serotonin reuptake inhibitor fluoxetine (FLX) is widely used to treat depression and anxiety disorders. Chronic FLX treatment reportedly induces cellular responses in the brain, including increased adult hippocampal and cortical neurogenesis and reversal of neuron maturation in the hippocampus, amygdala, and cortex. However, because most previous studies have used rodent models, it remains unclear whether these FLX-induced changes occur in the primate brain. To evaluate the effects of FLX in the primate brain, we used immunohistological methods to assess neurogenesis and the expression of neuronal maturity markers following chronic FLX treatment (3 mg/kg/day for 4 weeks) in adult marmosets (n= 3 per group). We found increased expression of doublecortin and calretinin, markers of immature neurons, in the hippocampal dentate gyrus of FLX-treated marmosets. Further, FLX treatment reduced parvalbumin expression and the number of neurons with perineuronal nets, which indicate mature fast-spiking interneurons, in the hippocampus, but not in the amygdala or cerebral cortex. We also found that FLX treatment increased the generation of cortical interneurons; however, significant up-regulation of adult hippocampal neurogenesis was not observed in FLX-treated marmosets. These results suggest that dematuration of hippocampal neurons and increased cortical neurogenesis may play roles in FLX-induced effects and/or side effects. Our results are consistent with those of previous studies showing hippocampal dematuration and increased cortical neurogenesis in FLX-treated rodents. In contrast, FLX did not affect hippocampal neurogenesis or dematuration of interneurons in the amygdala and cerebral cortex.

収録刊行物

• Molecular brain

  Molecular brain 12 (1), 69-, 2019-12

  Springer Nature

キーワード

• Cellular and Molecular Neuroscience
• Molecular Biology

詳細情報

• CRID: 1051693803359585152
• NII論文ID: 120006895413
• ISSN: 17566606
• DOI: 10.1186/s13041-019-0489-5
• HANDLE: 2433/255647
• Web Site: http://link.springer.com/content/pdf/10.1186/s13041-019-0489-5.pdf
• Web Site: http://link.springer.com/article/10.1186/s13041-019-0489-5/fulltext.html
• 本文言語コード: en
• 資料種別: journal article
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