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Ca 2+ entry through TRPC1 channels contributes to intracellular Ca 2+ dynamics and consequent glutamate release from rat astrocytes
Author(s) -
Malarkey Erik B.,
Ni Yingchun,
Parpura Vladimir
Publication year - 2008
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.20656
Subject(s) - biology , intracellular , glutamate receptor , astrocyte , trpc1 , biophysics , neuroscience , microbiology and biotechnology , biochemistry , ion channel , central nervous system , receptor
Astrocytes can respond to a variety of stimuli by elevating their cytoplasmic Ca 2+ concentration and can in turn release glutamate to signal adjacent neurons. The majority of this Ca 2+ is derived from internal stores while a portion also comes from outside of the cell. Astrocytes use Ca 2+ entry through store‐operated Ca 2+ channels to refill their internal stores. Therefore, we investigated what role this store‐operated Ca 2+ entry plays in astrocytic Ca 2+ responses and subsequent glutamate release. Astrocytes express canonical transient receptor potential (TRPC) channels that have been implicated in mediating store‐operated Ca 2+ entry. Here, we show that astrocytes in culture and freshly isolated astrocytes from visual cortex express TRPC1, TRPC4, and TRPC5. Indirect immunocytochemistry reveals that these proteins are present throughout the cell; the predominant expression of functionally tested TRPC1, however, is on the plasma membrane. Labeling in freshly isolated astrocytes reveals changes in TRPC expression throughout development. Using an antibody against TRPC1 we were able to block the function of TRPC1 channels and determine their involvement in mechanically and agonist‐evoked Ca 2+ entry in cultured astrocytes. Blocking TRPC1 was also found to reduce mechanically induced Ca 2+ ‐dependent glutamate release. These data indicate that Ca 2+ entry through TRPC1 channels contributes to Ca 2+ signaling in astrocytes and the consequent glutamate release from these cells. © 2008 Wiley‐Liss, Inc.