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BMC Research Notes

, 4:96

First Online: 31 March 2011Received: 01 December 2010Accepted: 31 March 2011DOI: 10.1186-1756-0500-4-96

Cite this article as: Warnock, G.I. & Steckler, T. BMC Res Notes 2011 4: 96. doi:10.1186-1756-0500-4-96


BackgroundRestraint stress in rodents has been reported to activate the hypothalamic-pituitary-adrenocortical HPA axis and to increase c-fos expression in regions that express components of the corticotropin-releasing factor CRF system. We have previously reported that acute central administration of CRF increased a measure of relative local cerebral glucose utilization LCGU, a measure of neuronal activity in specific brain regions, and activated the HPA axis in mice. It was hypothesized that the involvement of the CRF system in the stress response would lead to similar changes in relative LCGU after restraint stress. In the present studies the effect of restraint stress on relative LCGU and on the HPA axis in C57BL-6N mice were examined.

FindingsRestraint stress activated the HPA axis in a restraint-duration dependent manner, but in contrast to the reported effects of CRF, significantly decreased relative LCGU in frontal cortical, thalamic, hippocampal and temporal dissected regions. These findings support evidence that stressors enforcing limited physical activity reduce relative LCGU, in contrast to high activity stressors such as swim stress.

ConclusionsIn conclusion, the present studies do not support the hypothesis that stress-induced changes in relative LCGU are largely mediated by the CRF system. Further studies will help to delineate the role of the CRF system in the early phases of the relative LCGU response to stress and investigate the role of other neurotransmitter systems in this response.

Electronic supplementary materialThe online version of this article doi:10.1186-1756-0500-4-96 contains supplementary material, which is available to authorized users.

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Autor: Geoff I Warnock - Thomas Steckler


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