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Homozygous GAD65 and heterozygous GAD67 knock-out mice reveal normal retinal development and maintenance despite reduced amounts of GABA

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Acknowledgments

The authors thank the Department of Morphological Brain Science, Kyoto University, Japan for the hospitality to CAM during his sabbatical.

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Authors and Affiliations

  1. Department of Anatomy, Carl Gustav Carus Medical Faculty, Technical University Dresden, 01307, Dresden, Germany

    Christian Albrecht May

  2. Department of Morphological Brain Science, Kyoto University, Yoshida-Konoe-cho, Sakyo-ku, Kyoto, 606-8501, Japan

    Kouichi Nakamura & Fumino Fujiyama

  3. Department of Visual Neuroscience, Research Institute of Environmental Medicine, Nagoya University, Nagoya, 464-8601, Japan

    Yukio Komatsu

  4. Department of Genetic and Behavioral Neuroscience, Gunma University Graduate School of Medicine and SORST, JST, Maebashi, 371-8511, Japan

    Yuchio Yanagawa

Authors
  1. Christian Albrecht May
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  2. Kouichi Nakamura
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  3. Fumino Fujiyama
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  4. Yukio Komatsu
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  5. Yuchio Yanagawa
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Corresponding author

Correspondence to Christian Albrecht May.

Additional information

This research was supported by Johannes and Frieda Marohn Stiftung, Erlangen, and a Grant-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science, and Technology of Japan.

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May, C.A., Nakamura, K., Fujiyama, F. et al. Homozygous GAD65 and heterozygous GAD67 knock-out mice reveal normal retinal development and maintenance despite reduced amounts of GABA. Acta Neuropathol 113, 101–103 (2007). https://doi.org/10.1007/s00401-006-0157-6

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  • DOI: https://doi.org/10.1007/s00401-006-0157-6

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