Impaired motor coordination and persistent multiple climbing fiber innervation of cerebellar Purkinje cells in mice lacking Gαq

Stefan Offermanns, Kouichi Hashimoto, Masahiko Watanabe, William Sun, Hideo Kurihara, Richard F. Thompson, Yoshiro Inoue, Masanobu Kano, Melvin I. Simon

doi:10.1073/pnas.94.25.14089

Impaired motor coordination and persistent multiple climbing fiber innervation of cerebellar Purkinje cells in mice lacking Gαq

DOI Web Site 被引用文献29件

Stefan Offermanns

Division of Biology 147-75, California Institute of Technology, Pasadena, CA 91125; Laboratory for Cellular Neurophysiology, Brain Science Institute, RIKEN Wako-shi, Saitama 351-01, Japan; Department of Anatomy, Hokkaido University School of Medicine, Sapporo 060, Japan; Neuroscience Program, University of Southern California, University Park, Los Angeles, CA 90089-2520; and Department of Physiology, Jichi Medical School, Minamikawachi-machi, Tochigi-ken 329-04, Japan
Kouichi Hashimoto

Division of Biology 147-75, California Institute of Technology, Pasadena, CA 91125; Laboratory for Cellular Neurophysiology, Brain Science Institute, RIKEN Wako-shi, Saitama 351-01, Japan; Department of Anatomy, Hokkaido University School of Medicine, Sapporo 060, Japan; Neuroscience Program, University of Southern California, University Park, Los Angeles, CA 90089-2520; and Department of Physiology, Jichi Medical School, Minamikawachi-machi, Tochigi-ken 329-04, Japan
Masahiko Watanabe

Division of Biology 147-75, California Institute of Technology, Pasadena, CA 91125; Laboratory for Cellular Neurophysiology, Brain Science Institute, RIKEN Wako-shi, Saitama 351-01, Japan; Department of Anatomy, Hokkaido University School of Medicine, Sapporo 060, Japan; Neuroscience Program, University of Southern California, University Park, Los Angeles, CA 90089-2520; and Department of Physiology, Jichi Medical School, Minamikawachi-machi, Tochigi-ken 329-04, Japan
William Sun

Division of Biology 147-75, California Institute of Technology, Pasadena, CA 91125; Laboratory for Cellular Neurophysiology, Brain Science Institute, RIKEN Wako-shi, Saitama 351-01, Japan; Department of Anatomy, Hokkaido University School of Medicine, Sapporo 060, Japan; Neuroscience Program, University of Southern California, University Park, Los Angeles, CA 90089-2520; and Department of Physiology, Jichi Medical School, Minamikawachi-machi, Tochigi-ken 329-04, Japan
Hideo Kurihara

Division of Biology 147-75, California Institute of Technology, Pasadena, CA 91125; Laboratory for Cellular Neurophysiology, Brain Science Institute, RIKEN Wako-shi, Saitama 351-01, Japan; Department of Anatomy, Hokkaido University School of Medicine, Sapporo 060, Japan; Neuroscience Program, University of Southern California, University Park, Los Angeles, CA 90089-2520; and Department of Physiology, Jichi Medical School, Minamikawachi-machi, Tochigi-ken 329-04, Japan
Richard F. Thompson

Division of Biology 147-75, California Institute of Technology, Pasadena, CA 91125; Laboratory for Cellular Neurophysiology, Brain Science Institute, RIKEN Wako-shi, Saitama 351-01, Japan; Department of Anatomy, Hokkaido University School of Medicine, Sapporo 060, Japan; Neuroscience Program, University of Southern California, University Park, Los Angeles, CA 90089-2520; and Department of Physiology, Jichi Medical School, Minamikawachi-machi, Tochigi-ken 329-04, Japan
Yoshiro Inoue

Division of Biology 147-75, California Institute of Technology, Pasadena, CA 91125; Laboratory for Cellular Neurophysiology, Brain Science Institute, RIKEN Wako-shi, Saitama 351-01, Japan; Department of Anatomy, Hokkaido University School of Medicine, Sapporo 060, Japan; Neuroscience Program, University of Southern California, University Park, Los Angeles, CA 90089-2520; and Department of Physiology, Jichi Medical School, Minamikawachi-machi, Tochigi-ken 329-04, Japan
Masanobu Kano

Division of Biology 147-75, California Institute of Technology, Pasadena, CA 91125; Laboratory for Cellular Neurophysiology, Brain Science Institute, RIKEN Wako-shi, Saitama 351-01, Japan; Department of Anatomy, Hokkaido University School of Medicine, Sapporo 060, Japan; Neuroscience Program, University of Southern California, University Park, Los Angeles, CA 90089-2520; and Department of Physiology, Jichi Medical School, Minamikawachi-machi, Tochigi-ken 329-04, Japan
Melvin I. Simon

Division of Biology 147-75, California Institute of Technology, Pasadena, CA 91125; Laboratory for Cellular Neurophysiology, Brain Science Institute, RIKEN Wako-shi, Saitama 351-01, Japan; Department of Anatomy, Hokkaido University School of Medicine, Sapporo 060, Japan; Neuroscience Program, University of Southern California, University Park, Los Angeles, CA 90089-2520; and Department of Physiology, Jichi Medical School, Minamikawachi-machi, Tochigi-ken 329-04, Japan

抄録

<jats:p> Mice lacking the α-subunit of the heterotrimeric guanine nucleotide binding protein G <jats:sub>q</jats:sub> (Gα <jats:sub>q</jats:sub> ) are viable but suffer from ataxia with typical signs of motor discoordination. The anatomy of the cerebellum is not overtly disturbed, and excitatory synaptic transmission from parallel fibers to cerebellar Purkinje cells (PCs) and from climbing fibers (CFs) to PCs is functional. However, about 40% of adult Gα <jats:sub>q</jats:sub> mutant PCs remain multiply innervated by CFs because of a defect in regression of supernumerary CFs in the third postnatal week. Evidence is provided suggesting that Gα <jats:sub>q</jats:sub> is part of a signaling pathway that is involved in the elimination of multiple CF innervation during this period. </jats:p>

収録刊行物

Proceedings of the National Academy of Sciences

Proceedings of the National Academy of Sciences 94 (25), 14089-14094, 1997-12-09

Proceedings of the National Academy of Sciences