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Front Mol Neurosci. 2015 Nov 16;8:68. doi: 10.3389/fnmol.2015.00068. eCollection 2015.

Early Life Stress Effects on Glucocorticoid-BDNF Interplay in the Hippocampus.

Author information

1
Traumatic Stress Studies Division and Laboratory of Molecular Neuropsychiatry, Department of Psychiatry, Icahn School of Medicine at Mount Sinai New York, NY, USA ; Mental Health Patient Care Center, James J. Peters Veterans Affairs Medical Center Bronx, NY, USA.
2
Department of Medical Pharmacology, Leiden Academic Centre for Drug Research Leiden, Netherlands ; Department of Endocrinology and Metabolism, Leiden University Medical Center, Leiden University Leiden, Netherlands.
3
Traumatic Stress Studies Division and Laboratory of Molecular Neuropsychiatry, Department of Psychiatry, Icahn School of Medicine at Mount Sinai New York, NY, USA ; Mental Health Patient Care Center, James J. Peters Veterans Affairs Medical Center Bronx, NY, USA ; Department of Neuroscience, Icahn School of Medicine at Mount Sinai New York, NY, USA.
4
Department of Psychiatry, New York University School of Medicine New York, NY, USA.
5
Departments of Cell Biology, Physiology and Neuroscience, and Psychiatry, Skirball Institute of Biomolecular Medicine, New York University New York, NY, USA.

Abstract

Early life stress (ELS) is implicated in the etiology of multiple psychiatric disorders. Important biological effects of ELS are manifested in stress-susceptible regions of the hippocampus and are partially mediated by long-term effects on glucocorticoid (GC) and/or neurotrophin signaling pathways. GC-signaling mediates the regulation of stress response to maintain homeostasis, while neurotrophin signaling plays a key role in neuronal outgrowth and is crucial for axonal guidance and synaptic integrity. The neurotrophin and GC-signaling pathways co-exist throughout the central nervous system (CNS), particularly in the hippocampus, which has high expression levels of glucocorticoid-receptors (GR) and mineralocorticoid-receptors (MR) as well as brain-derived neurotrophic factor (BDNF) and its receptor, tropomyosin-related kinase receptor B (TrkB). This review addresses the effects of ELS paradigms on GC- and BDNF-dependent mechanisms and their crosstalk in the hippocampus, including potential implications for the pathogenesis of common stress-related disorders.

KEYWORDS:

BDNF; HPA-axis; TrkB; early life stress; glucocorticoid; glucocorticoid receptor; hippocampus

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