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Lateral diffusion of inositol 1,4,5‐trisphosphate receptor type 1 in Purkinje cells is regulated by calcium and actin filaments
Author(s) -
Fukatsu Kazumi,
Bannai Hiroko,
Inoue Takafumi,
Mikoshiba Katsuhiko
Publication year - 2010
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2010.06885.x
Subject(s) - microbiology and biotechnology , quisqualic acid , fluorescence recovery after photobleaching , biophysics , actin remodeling of neurons , inositol , chemistry , actin , actin cytoskeleton , biology , receptor , glutamate receptor , cytoskeleton , biochemistry , cell , membrane , ampa receptor
J. Neurochem. (2010) 114 , 1720–1733. Abstract Inositol 1,4,5‐trisphosphate receptor type 1 (IP 3 R1) is an intracellular Ca 2+ release channel that plays crucial roles in the functions of Purkinje cells. The dynamics of IP 3 R1 on the endoplasmic reticulum membrane and the distribution of IP 3 R1 in neurons are thought to be important for the spatial regulation of Ca 2+ release. In this study, we analyzed the lateral diffusion of IP 3 R1 in Purkinje cells in cerebellar slice cultures using fluorescence recovery after photobleaching. In the dendrites of Purkinje cells, IP 3 R1 showed lateral diffusion with an effective diffusion constant of approximately 0.30 μm 2 /s, and the diffusion of IP 3 R1 was negatively regulated by actin filaments. We found that actin filaments were also involved in the regulation of IP 3 R1 diffusion in the spine of Purkinje cells. Glutamate or quisqualic acid stimulation, which activates glutamate receptors and leads to a Ca 2+ transient in Purkinje cells, decreased the diffusion of IP 3 R1 and increased the density of actin in spines. These findings indicate that the neuronal activity‐dependent augmentation of actin contributes to the stabilization of IP 3 R1 in spines.