| Repeated stress impairs endocannabinoid signaling in the paraventricular nucleus of the hypothalamus. | |
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MedLine Citation:
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PMID: 20720126 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Endocannabinoids (eCBs) are ubiquitous retrograde signaling molecules in the nervous system that are recruited in response to robust neuronal activity or the activation of postsynaptic G-protein-coupled receptors. Physiologically, eCBs have been implicated as important mediators of the stress axis and they may contribute to the rapid feedback inhibition of the hypothalamic-pituitary-adrenal axis (HPA) by circulating corticosteroids (CORTs). Understanding the relationship between stress and eCBs, however, is complicated by observations that eCB signaling is itself sensitive to stress. The mechanisms that link stress to changes in synaptic eCB signaling and the impact of these changes on CORT-mediated negative feedback have not been resolved. Here, we show that repetitive immobilization stress, in juvenile male rats, causes a functional downregulation of CB(1) receptors in the paraventricular nucleus of the hypothalamus (PVN). This loss of CB(1) receptor signaling, which requires the activation of genomic glucocorticoid receptors, impairs both activity and receptor-dependent eCB signaling at GABA and glutamate synapses on parvocellular neuroendocrine cells in PVN. Our results provide a plausible mechanism for how stress can lead to alterations in CORT-mediated negative feedback and may contribute to the development of plasticity of HPA responses. |
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Authors:
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Jaclyn I Wamsteeker; J Brent Kuzmiski; Jaideep S Bains |
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Publication Detail:
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Type: In Vitro; Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: The Journal of neuroscience : the official journal of the Society for Neuroscience Volume: 30 ISSN: 1529-2401 ISO Abbreviation: J. Neurosci. Publication Date: 2010 Aug |
Date Detail:
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Created Date: 2010-08-19 Completed Date: 2010-09-03 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8102140 Medline TA: J Neurosci Country: United States |
Other Details:
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Languages: eng Pagination: 11188-96 Citation Subset: IM |
Affiliation:
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Hotchkiss Brain Institute and Department of Physiology and Pharmacology, University of Calgary, Calgary, Alberta T2N 4N1, Canada. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Chronic Disease Endocannabinoids / metabolism* Hippocampus / physiopathology Inhibitory Postsynaptic Potentials Male Neural Inhibition / physiology Neuroendocrine Cells / physiology Neurons / physiology Paraventricular Hypothalamic Nucleus / physiopathology* Presynaptic Terminals / physiology Rats Rats, Sprague-Dawley Receptor, Cannabinoid, CB1 / metabolism Receptors, G-Protein-Coupled / metabolism Restraint, Physical Signal Transduction* Stress, Psychological / physiopathology* Synapses / physiology gamma-Aminobutyric Acid / metabolism |
| Grant Support | |
ID/Acronym/Agency:
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//Canadian Institutes of Health Research |
| Chemical | |
Reg. No./Substance:
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0/Endocannabinoids; 0/Receptor, Cannabinoid, CB1; 0/Receptors, G-Protein-Coupled; 56-12-2/gamma-Aminobutyric Acid |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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