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Corticosterone Regulates pERK1/2 Map Kinase in a Chronic Depression Model
Author(s) -
Gourley Shan L.,
Wu Florence J.,
Taylor Jane R.
Publication year - 2008
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1410.076
Subject(s) - dentate gyrus , prefrontal cortex , hippocampus , hippocampal formation , neuroscience , corticosterone , neurotrophin , antidepressant , extracellular , kinase , neurotrophic factors , neurotransmitter , chronic stress , psychology , neuroplasticity , brain derived neurotrophic factor , endocrinology , receptor , biology , medicine , microbiology and biotechnology , cognition , hormone , central nervous system
Neurotransmitter‐ or neurotrophin‐regulated intracellular signaling in the hippocampus is hypothesized to contribute to depression and antidepressant (ADT) efficacy. Extracellular signal‐regulated kinase 1/2 (ERK1/2) is downstream of several receptor types and regulates transcriptional activity of many targets; ERK1/2 may thereby influence mood and affect. Using a novel, ADT‐sensitive depression model in mice, we show that prior corticosterone exposure decreases motivated behavior, sucrose consumption, and pERK1/2 in the dentate gyrus, but not in CA1/CA3. Notably, prefrontal cortical targets were also regulated. Our data suggest ADTs restore hippocampal pERK1/2 after stress‐related insult, and potentially reveal a novel role for prefrontal neurotrophins in depressive‐like symptomology.
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