Disruption of the midkine gene (Mdk) resulted in altered expression of a calcium binding protein in the hippocampus of infant mice and their abnormal behaviour

Eishin Nakamura, Kenji Kadomatsu, Shigeki Yuasa, Hisako Muramatsu, Takayoshi Mamiya, Toshitaka Nabeshima, Qi Wen Fan, Kazuhiro Ishiguro, Tadahiko Igakura, Shuichiro Matsubara, Tadashi Kaname, Mitsuru Horiba, Hidehiko Saito, Takashi Muramatsu

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114 Citations (Scopus)

Abstract

Background: Midkine (MK) is a growth factor implicated in the development and repair of various tissues, especially neural tissues. However, its in vivo function has not been clarified. Results: Knockout mice lacking the MK gene (Mdk) showed no gross abnormalities. We closely analysed postnatal brain development in Mdk(-/-) mice using calcium binding proteins as markers to distinguish neuronal subpopulations. Intense and prolonged calretinin expression was found in the dentate gyrus granule cell layer of the hippocampus of infant Mdk(-/-) mice. In infant Mdk(+/+) mice, calretinin expression in the granule cell layer was weaker, and had disappeared by 4 weeks after birth, when calretinin expression still persisted in Mdk(-/-) mice. Furthermore, 4 weeks after birth, Mdk(-/-) mice showed a deficit in their working memory, as revealed by a Y-maze test, and had an increased anxiety, as demonstrated by the elevated plus-maze test. Conclusion: Midkine plays an important role in the regulation of postnatal development of the hippocampus.

Original languageEnglish
Pages (from-to)811-812
Number of pages2
JournalGenes to Cells
Volume3
Issue number12
DOIs
Publication statusPublished - 1998

All Science Journal Classification (ASJC) codes

  • Genetics
  • Cell Biology

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    Nakamura, E., Kadomatsu, K., Yuasa, S., Muramatsu, H., Mamiya, T., Nabeshima, T., Fan, Q. W., Ishiguro, K., Igakura, T., Matsubara, S., Kaname, T., Horiba, M., Saito, H., & Muramatsu, T. (1998). Disruption of the midkine gene (Mdk) resulted in altered expression of a calcium binding protein in the hippocampus of infant mice and their abnormal behaviour. Genes to Cells, 3(12), 811-812. https://doi.org/10.1046/j.1365-2443.1998.00231.x