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Calcium signaling and glucose response is different in adult compared to neonatal rat astrocytes (1177.7)
Author(s) -
Rarick Kevin,
Eisenhauer Jessica,
Harder David
Publication year - 2014
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.28.1_supplement.1177.7
Subject(s) - glutamate receptor , astrocyte , biology , endocrinology , medicine , calcium signaling , metabotropic glutamate receptor 5 , receptor , metabotropic glutamate receptor , calcium , neuroglia , microbiology and biotechnology , central nervous system
Much of our mechanistic understanding of astrocytes comes from neonatal cells which may not represent the mature glial phenotype. We sought to determine if neonatal and adult astrocytes respond similarly when challenged with high glucose. Neonatal and adult rat astrocytes were cultured in 5.5 mM low glucose DMEM (LG) and then maintained in LG or switched to 25 mM high glucose DMEM (HG) for two weeks. A developmental decrease was observed in expression of the inositol trisphosphate receptor (IP3R) and the metabotropic glutamate 5 receptor (mGluR5). The L‐type calcium channel (CaV1.2) was only expressed in adult astrocytes. Adult and neonatal astrocytes both responded to HG with increased mGluR5 and decreased IP3R protein expression. Adult astrocytes also increased CaV1.2 expression following HG. Neonatal astrocytes had a greater magnitude and rate of rise of [Ca 2+ ]i in response to ATP and glutamate compared to adult astrocytes. The [Ca 2+ ]i responses to ATP and glutamate were similarly affected by HG, although adult astrocytes demonstrated minimal response to glutamate in all conditions. Cell viability decreased only in adult astrocytes following HG. These results suggest HG alters calcium signaling in astrocytes and developmental differences may exist in downstream pro‐survival signaling. The response of adult glia in specific disease paradigms may not be accurately reflected when using neonatal cells. Grant Funding Source : Supported by T32 HL007792, R01 HL033833, R01 HL 092105, and R01 HL105997