Document Detail


Repeated stress impairs endocannabinoid signaling in the paraventricular nucleus of the hypothalamus.
MedLine Citation:
PMID:  20720126     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Jaclyn I Wamsteeker; J Brent Kuzmiski; Jaideep S Bains
Related Documents :
17055146 - Trans-activation, cis-activation and signal selection of gonadotropin receptors.
21105826 - Bayes-optimal chemotaxis.
20404556 - New perspective in ethylene signaling.
7832496 - Possible mechanisms for the powerful actions of neuropeptides.
1369346 - Designing peptide and protein ligands for biological receptors.
8265816 - Human im-9 lymphoblasts as a model of the growth hormone-insulin-like growth factor axi...
Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
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:
Created Date:  2010-08-19     Completed Date:  2010-09-03     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8102140     Medline TA:  J Neurosci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  11188-96     Citation Subset:  IM    
Affiliation:
Hotchkiss Brain Institute and Department of Physiology and Pharmacology, University of Calgary, Calgary, Alberta T2N 4N1, Canada.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
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:
//Canadian Institutes of Health Research
Chemical
Reg. No./Substance:
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


Previous Document:  Implicit perceptual anticipation triggered by statistical learning.
Next Document:  Direction-selective ganglion cells show symmetric participation in retinal waves during development.