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BMC Res Notes. 2011 Mar 31;4:96. doi: 10.1186/1756-0500-4-96.

Stress-induced decreases in local cerebral glucose utilization in specific regions of the mouse brain.

BMC research notes

Geoff I Warnock, Thomas Steckler

Affiliations

  1. University of Liege, Cyclotron Research Center, Allée du 6 Août, 8, 4000 Liege, Belgium. [email protected].

PMID: 21453518 PMCID: PMC3076272 DOI: 10.1186/1756-0500-4-96

Abstract

BACKGROUND: Restraint 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.

FINDINGS: Restraint 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.

CONCLUSIONS: In 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.

References

  1. Neuroscience. 2003;122(1):1-4 - PubMed
  2. J Neurosci. 1993 Sep;13(9):3932-43 - PubMed
  3. Am J Physiol. 1990 Apr;258(4 Pt 1):G591-5 - PubMed
  4. J Biol Chem. 1954 Oct;210(2):581-95 - PubMed
  5. Behav Brain Res. 2009 Oct 12;203(1):43-7 - PubMed
  6. Physiol Behav. 1995 Oct;58(4):749-54 - PubMed
  7. J Comp Neurol. 1993 Jun 1;332(1):1-20 - PubMed
  8. Physiol Behav. 1985 Apr;34(4):595-9 - PubMed
  9. Brain Res. 1984 Jul 2;305(1):109-13 - PubMed
  10. Neuroendocrinology. 1988 Apr;47(4):329-34 - PubMed
  11. Am J Physiol. 1983 Mar;244(3):R363-7 - PubMed
  12. Pharmacol Res. 2000 Aug;42(2):171-6 - PubMed
  13. Neuroscience. 2007 Mar 30;145(3):1048-58 - PubMed
  14. J Cereb Blood Flow Metab. 1988 Oct;8(5):720-6 - PubMed
  15. Psychoneuroendocrinology. 1983;8(4):447-50 - PubMed
  16. Pharmacol Biochem Behav. 1978 Jul;9(1):21-6 - PubMed
  17. Brain Res. 1992 Oct 2;592(1-2):228-38 - PubMed
  18. Endocrinology. 1988 Jul;123(1):396-405 - PubMed
  19. Neurosci Lett. 2009 Feb 13;451(1):60-4 - PubMed
  20. Braz J Med Biol Res. 2001 Jan;34(1):111-6 - PubMed
  21. J Neurochem. 1977 May;28(5):897-916 - PubMed
  22. J Neurochem. 1991 Oct;57(4):1422-8 - PubMed
  23. Peptides. 2009 May;30(5):947-54 - PubMed
  24. Neuroscience. 2006;138(1):235-43 - PubMed
  25. Stress. 2005 Sep;8(3):199-211 - PubMed
  26. Proc Natl Acad Sci U S A. 1994 Oct 25;91(22):10625-9 - PubMed
  27. Endocrinology. 2004 Jan;145(1):351-9 - PubMed
  28. Perspect Biol Med. 1971 Winter;14(2):265-9 - PubMed
  29. Life Sci. 2006 Feb 16;78(12):1392-9 - PubMed
  30. Horm Behav. 1996 Dec;30(4):611-7 - PubMed
  31. J Neurochem. 1958 Dec;3(2):185-205 - PubMed
  32. Neuroendocrinology. 1990 Jul;52(1):57-64 - PubMed
  33. Endocrinology. 1994 Apr;134(4):1924-31 - PubMed

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