| Decreased heat tolerance is associated with hypothalamo-pituitary-adrenocortical axis impairment. | |
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MedLine Citation:
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PMID: 17531395 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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When rats are exposed to heat, they adapt themselves to the stressor with a wide inter-individual variability. Such differences in heat tolerance may be related to particularities in the hypothalamo-pituitary-adrenocortical (HPA) axis activation. To further this hypothesis, 80 rats instrumented with a telemetric device for abdominal temperature (Tabd) measurement were separated into two groups. Sixty-eight rats were exposed during 90 min at an ambient temperature of 40 degrees C, and 12 rats to an ambient temperature of 22 degrees C. Heat-exposed rats were then divided into three groups using the a posteriori k-means clustering method according to their Tabd level at the end of heat exposure. Heat tolerant rats (Tol, n=30) exhibiting the lowest Tabd showed a slight dehydration, a moderate triglyceride mobilization, but the highest plasma adrenocorticotropic-hormone (ACTH) and corticosterone levels. Conversely, heat exhausted rats (HE, n=14) presented the highest Tabd, a higher degree of dehydration, a greater metabolic imbalance with the lowest plasma triglyceride level and the highest lactate concentration, as well as a lowest plasma corticosterone and ACTH levels. The fact that the proopiomelanocortin (POMC) mRNA content within the pituitary was low despite of a high c-fos mRNA level is also relevant. Current inflammatory processes in HE rats were underlined by lower inhibitory factor kappaBalpha (IkappaBalpha) mRNA and higher tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) mRNA. In conclusion, data show that intolerance to heat exposure is associated to an HPA axis impairment, possibly related to changes occurring in the IkappaBalpha and TNF-alpha mRNA levels. |
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Authors:
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V Michel; A Peinnequin; A Alonso; A Buguet; R Cespuglio; F Canini |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2007-05-24 |
Journal Detail:
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Title: Neuroscience Volume: 147 ISSN: 0306-4522 ISO Abbreviation: Neuroscience Publication Date: 2007 Jun |
Date Detail:
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Created Date: 2007-06-19 Completed Date: 2007-09-18 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 7605074 Medline TA: Neuroscience Country: United States |
Other Details:
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Languages: eng Pagination: 522-31 Citation Subset: IM |
Affiliation:
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Département des Facteurs Humains, Pôle de Neurophysiologie du Stress, Centre de Recherches du Service de Santé des Armées Emile Pardé, 24 Avenue des Maquis du Grésivaudan, F-38702 La Tronche Cédex, France. vmichel@crssa.net |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adrenocorticotropic Hormone
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blood Animals Calcium Signaling / physiology Corticosterone / blood Corticotropin-Releasing Hormone / biosynthesis, genetics Gene Expression / physiology Genes, Immediate-Early / genetics HSP70 Heat-Shock Proteins / biosynthesis, genetics Heat Stress Disorders / physiopathology* Hematocrit Hypothalamo-Hypophyseal System / physiopathology* Inflammation Mediators / metabolism Male Pituitary-Adrenal System / physiopathology* Pro-Opiomelanocortin / biosynthesis, genetics RNA, Messenger / analysis, biosynthesis Rats Rats, Sprague-Dawley Reverse Transcriptase Polymerase Chain Reaction Telemetry Transcription Factors / biosynthesis, genetics |
| Chemical | |
Reg. No./Substance:
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0/HSP70 Heat-Shock Proteins; 0/Inflammation Mediators; 0/MCIP-1 protein, rat; 0/RNA, Messenger; 0/Transcription Factors; 50-22-6/Corticosterone; 66796-54-1/Pro-Opiomelanocortin; 9002-60-2/Adrenocorticotropic Hormone; 9015-71-8/Corticotropin-Releasing Hormone |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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