Document Detail

Decreased heat tolerance is associated with hypothalamo-pituitary-adrenocortical axis impairment.
MedLine Citation:
PMID:  17531395     Owner:  NLM     Status:  MEDLINE    
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.
V Michel; A Peinnequin; A Alonso; A Buguet; R Cespuglio; F Canini
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2007-05-24
Journal Detail:
Title:  Neuroscience     Volume:  147     ISSN:  0306-4522     ISO Abbreviation:  Neuroscience     Publication Date:  2007 Jun 
Date Detail:
Created Date:  2007-06-19     Completed Date:  2007-09-18     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7605074     Medline TA:  Neuroscience     Country:  United States    
Other Details:
Languages:  eng     Pagination:  522-31     Citation Subset:  IM    
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.
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MeSH Terms
Adrenocorticotropic Hormone / blood
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*
Hypothalamo-Hypophyseal System / physiopathology*
Inflammation Mediators / metabolism
Pituitary-Adrenal System / physiopathology*
Pro-Opiomelanocortin / biosynthesis,  genetics
RNA, Messenger / analysis,  biosynthesis
Rats, Sprague-Dawley
Reverse Transcriptase Polymerase Chain Reaction
Transcription Factors / biosynthesis,  genetics
Reg. No./Substance:
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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