Open AccessPCB-95 Modulates the Calcium-Dependent Signaling Pathway Responsible for Activity-Dependent Dendritic Growth
Author(s) -
Gary A. Wayman,
Diptiman D. Bose,
Dongren Yang,
Atom J. Lesiak,
Donald A. Bruun,
Soren Impey,
Veronica A. Ledoux,
Isaac N. Pessah,
Pamela J. Lein
Publication year - 2012
Publication title -
environmental health perspectives
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.257
H-Index - 282
eISSN - 1552-9924
pISSN - 0091-6765
DOI - 10.1289/ehp.1104833
Subject(s) - creb , ryanodine receptor , microbiology and biotechnology , dendritic spine , chemistry , signal transduction , hippocampal formation , calcium signaling , calmodulin , mapk/erk pathway , biology , transcription factor , calcium , intracellular , neuroscience , biochemistry , gene , organic chemistry
Non-dioxin-like (NDL) polychlorinated biphenyls (PCBs) promote dendritic growth in hippocampal neurons via ryanodine receptor (RyR)-dependent mechanisms; however, downstream signaling events that link enhanced RyR activity to dendritic growth are unknown. Activity-dependent dendritic growth, which is a critical determinant of neuronal connectivity in the developing brain, is mediated by calcium ion (Ca(2+))-dependent activation of Ca(2+)/calmodulin kinase-I (CaMKI), which triggers cAMP response element binding protein (CREB)-dependent Wnt2 transcription. RyRs regulate the spatiotemporal dynamics of intracellular Ca(2+) signals, but whether RyRs promote dendritic growth via modulation of this signaling pathway is not known.
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