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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
29
pubmed:dateCreated
2011-7-21
pubmed:abstractText
The mechanisms subserving the ability of glucocorticoid signaling within the medial prefrontal cortex (mPFC) to terminate stress-induced activation of the hypothalamic-pituitary-adrenal (HPA) axis are not well understood. We report that antagonism of the cannabinoid CB(1) receptor locally within the mPFC prolonged corticosterone secretion following cessation of stress in rats. Mice lacking the CB(1) receptor exhibited a similar prolonged response to stress. Exposure of rats to stress produced an elevation in the endocannabinoid 2-arachidonoylglycerol within the mPFC that was reversed by pretreatment with the glucocorticoid receptor antagonist RU-486 (20 mg/kg). Electron microscopic and electrophysiological data demonstrated the presence of CB(1) receptors in inhibitory-type terminals impinging upon principal neurons within layer V of the prelimbic region of the mPFC. Bath application of corticosterone (100 nm) to prefrontal cortical slices suppressed GABA release onto principal neurons in layer V of the prelimbic region, when examined 1 h later, which was prevented by application of a CB(1) receptor antagonist. Collectively, these data demonstrate that the ability of stress-induced glucocorticoid signaling within mPFC to terminate HPA axis activity is mediated by a local recruitment of endocannabinoid signaling. Endocannabinoid activation of CB(1) receptors decreases GABA release within the mPFC, likely increasing the outflow of the principal neurons of the prelimbic region to contribute to termination of the stress response. These data support a model in which endocannabinoid signaling links glucocorticoid receptor engagement to activation of corticolimbic relays that inhibit corticosterone secretion.
pubmed:grant
http://linkedlifedata.com/resource/pubmed/grant/, http://linkedlifedata.com/resource/pubmed/grant/5 T32 DA7274-19, http://linkedlifedata.com/resource/pubmed/grant/DA011322, http://linkedlifedata.com/resource/pubmed/grant/DA021696, http://linkedlifedata.com/resource/pubmed/grant/DA024741, http://linkedlifedata.com/resource/pubmed/grant/DA09155, http://linkedlifedata.com/resource/pubmed/grant/K05 DA021696-05, http://linkedlifedata.com/resource/pubmed/grant/MH40342, http://linkedlifedata.com/resource/pubmed/grant/MH41256, http://linkedlifedata.com/resource/pubmed/grant/R01 DA004600-22, http://linkedlifedata.com/resource/pubmed/grant/R01 DA009155-12, http://linkedlifedata.com/resource/pubmed/grant/R01 DA011322-13, http://linkedlifedata.com/resource/pubmed/grant/R01 DA024741-05, http://linkedlifedata.com/resource/pubmed/grant/R01 MH040342-28, http://linkedlifedata.com/resource/pubmed/grant/R01 MH041256-25
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/2-arachidonylglycerol, http://linkedlifedata.com/resource/pubmed/chemical/AM 251, http://linkedlifedata.com/resource/pubmed/chemical/Arachidonic Acids, http://linkedlifedata.com/resource/pubmed/chemical/Calcium-Calmodulin-Dependent..., http://linkedlifedata.com/resource/pubmed/chemical/Corticosterone, http://linkedlifedata.com/resource/pubmed/chemical/Glycerides, http://linkedlifedata.com/resource/pubmed/chemical/Hormone Antagonists, http://linkedlifedata.com/resource/pubmed/chemical/Mifepristone, http://linkedlifedata.com/resource/pubmed/chemical/Piperidines, http://linkedlifedata.com/resource/pubmed/chemical/Pyrazoles, http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Cannabinoid, CB1, http://linkedlifedata.com/resource/pubmed/chemical/gamma-Aminobutyric Acid
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1529-2401
pubmed:author
pubmed:issnType
Electronic
pubmed:day
20
pubmed:volume
31
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
10506-15
pubmed:dateRevised
2011-11-4
pubmed:meshHeading
pubmed-meshheading:21775596-Animals, pubmed-meshheading:21775596-Arachidonic Acids, pubmed-meshheading:21775596-Calcium-Calmodulin-Dependent Protein Kinase Type 2, pubmed-meshheading:21775596-Corticosterone, pubmed-meshheading:21775596-Disease Models, Animal, pubmed-meshheading:21775596-Electric Stimulation, pubmed-meshheading:21775596-Freezing Reaction, Cataleptic, pubmed-meshheading:21775596-Glycerides, pubmed-meshheading:21775596-Hormone Antagonists, pubmed-meshheading:21775596-Long-Term Synaptic Depression, pubmed-meshheading:21775596-Male, pubmed-meshheading:21775596-Mice, pubmed-meshheading:21775596-Mice, Inbred C57BL, pubmed-meshheading:21775596-Mice, Inbred ICR, pubmed-meshheading:21775596-Mice, Knockout, pubmed-meshheading:21775596-Microscopy, Electron, Transmission, pubmed-meshheading:21775596-Mifepristone, pubmed-meshheading:21775596-Patch-Clamp Techniques, pubmed-meshheading:21775596-Piperidines, pubmed-meshheading:21775596-Prefrontal Cortex, pubmed-meshheading:21775596-Pyramidal Cells, pubmed-meshheading:21775596-Pyrazoles, pubmed-meshheading:21775596-Rats, pubmed-meshheading:21775596-Rats, Sprague-Dawley, pubmed-meshheading:21775596-Receptor, Cannabinoid, CB1, pubmed-meshheading:21775596-Signal Transduction, pubmed-meshheading:21775596-Stress, Psychological, pubmed-meshheading:21775596-gamma-Aminobutyric Acid
pubmed:year
2011
pubmed:articleTitle
Recruitment of prefrontal cortical endocannabinoid signaling by glucocorticoids contributes to termination of the stress response.
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