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The Role of Voltage‐Operated Calcium Channels in Astrocyte Reactivity
Author(s) -
Smith Jessica,
Paez Pablo
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.1021.5
Subject(s) - astrocyte , depolarization , calcium , astrogliosis , chemistry , voltage dependent calcium channel , potassium channel , verapamil , calcium channel , membrane potential , calcium activated potassium channel , microbiology and biotechnology , neuroscience , biophysics , biology , biochemistry , central nervous system , organic chemistry
Reactive astrogliosis is a universal response of astrocytes to brain injuries and diseases as diverse as trauma, infection, neurodegeneration, and ischemia. Reactive astrocytes undergo dramatic morphological changes (Wilhelmsson et al., 2006), and various alterations in gene expression have been observed (Sofroniew, 2009). It has long been debated whether reactive astrocytes are harmful or beneficial. In the past few years, both types of properties have been observed. Previous studies have shown that the plasma membranes of astrocytes depolarize when treated with high levels of potassium and this in turn activates voltage‐operated calcium channels. What we are looking to find out more about is the role that these channels play in astrocyte reactivity. We hypothesize that incubating primary astrocyte cultures with high levels of potassium will cause astrocytes to become reactive and that blocking the voltage‐operated calcium channels of these cells will inhibit their ability to become reactive. Our experiments involved incubating cell cultures for three days with different levels of potassium and performing immunocytochemistry with GFAP and S100 antibodies to determine the amount of reactivity. We found that high levels of potassium caused the astrocytes to become reactive and through the use of L‐type voltage‐operated calcium channel blockers Verapamil and Nifedipine, we were able to conclude that these channels are necessary for reactivity under these conditions. In summary, our results suggest that voltage‐operated calcium channels may play a fundamental role in the induction of reactive astrocytes, and indicate that the inhibition of these calcium channels may be an effective way to prevent astrocyte activation.