Atomic Force Microscopic Observation of Three-Dimensional Morphological Changes of Neurons When Stimulated by a Neurotransmitter.

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  • Hosono Tomoko
    Division of Biological Sciences, Graduate School of Science, Hokkaido University, Kita–ku, Sapporo 060–0810, Japan
  • Yamanaka Mari
    Division of Biological Sciences, Graduate School of Science, Hokkaido University, Kita–ku, Sapporo 060–0810, Japan
  • Tojima Takuro
    Division of Biological Sciences, Graduate School of Science, Hokkaido University, Kita–ku, Sapporo 060–0810, Japan
  • Yamane Yukako
    Division of Biological Sciences, Graduate School of Science, Hokkaido University, Kita–ku, Sapporo 060–0810, Japan
  • Sadamoto Hisayo
    Division of Biological Sciences, Graduate School of Science, Hokkaido University, Kita–ku, Sapporo 060–0810, Japan
  • Hatakeyama Dai
    Division of Biological Sciences, Graduate School of Science, Hokkaido University, Kita–ku, Sapporo 060–0810, Japan
  • Haga Hisashi
    Division of Physics, Graduate School of Science, Hokkaido University, Kita–ku, Sapporo 060–0810, Japan
  • Kawabata Kazushige
    Division of Physics, Graduate School of Science, Hokkaido University, Kita–ku, Sapporo 060–0810, Japan
  • Abe Kazuhiro
    Department of Anatomy, Hokkaido University Graduate School of Medicine, Kita–ku, Sapporo 060–8638, Japan
  • Ito Etsuro
    Division of Biological Sciences, Graduate School of Science, Hokkaido University, Kita–ku, Sapporo 060–0810, Japan

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As the first step in the study of morphological changes in neurons associated with their functional changes, we applied atomic force microscopy (AFM) for the observation of fine three-dimensional morphological changes in rat cerebellar granule cells stimulated by an agonist of glutamate receptors, N-methyl-d-aspartate (NMDA). The AFM revealed that NMDA changed the cross-sections of cell bodies from a trapezoid-like form to a triangle-like form within a minute. The fine hill-like structures on the top surfaces of the cell bodies became wider during the same period. These results were suggested to be induced by the depolymerization of filamentous actin triggered by the entry of Ca2+ via cation channels complexed with the activated NMDA receptors.

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