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Cited by 3,566

The DOI matches its Crossref record; 24 of the 24 references it cites were found in a registry or an index.

The Neuroendocrinology of Stress: A Never Ending Story

Lightman, S. L.·2008·Journal of Neuroendocrinology
DOI 10.1111/j.1365-2826.2008.01711.x
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Abstract

Evolutionary success depends on our ability to adapt to changing circumstances. The neuroendocrine response to stress is an excellent example of a plastic system that responds to threats to homeostasis and alters its output to meet current and expected future demands. At the level of the hypothalamus, the corticotroph secretagogues corticotrophin‐releasing hormone (CRH) and arginine vasopressin (AVP) respond rapidly to an acute stressor but, following chronic stress, they adapt with a reduction of CRH but a major increase in AVP. The release of CRH and AVP activates pro‐opiomelanocortin in anterior pituitary corticotroph cells and the release of adrenocorticotrophic hormone into peripheral blood from where it targets receptors in the adrenal cortex to release glucocorticoid hormones. These hormones (i.e. corticosterone in the rat and cortisol in man) are released in a pulsatile ultradian pattern which defines the normal circadian rhythm. The frequency of the pulses is increased under states of chronic stress, and in rats with genetically determined hyper‐responsiveness of the hypothalamic‐pituitary‐adrenal axis. Interestingly, neonatal influences can also programme alterations in ultradian rhythmicity, implicating epigenetic factors in its regulation. At the level of tissue receptors, the alteration in pattern of glucocorticoid ultradian rhythm has differential effects on mineralocorticoid receptor and glucocorticoid receptor (GR) binding to DNA and offers a mechanism for tissue specific responses to altered glucocorticoid dynamics. The effects of neonatal experience are not only seen at the level of CRH and GR regulation, but also are evident in behavioural responses to stress and in the responsiveness of brain stem serotonergic pathways, as measured by tryptophan hydroxylase mRNA in the brain stem.

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Show all 24 references

Research works printed but not linked: 18

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  2. 10.1073/pnas.86.23.9569 · DOI · Paper page
  3. 10.1113/jphysiol.1988.sp017261 · DOI
  4. 10.1038/328643a0 · DOI
  5. 10.1210/en.130.3.1394 · DOI
  6. 10.1111/j.1476-5381.1995.tb15089.x · DOI
  7. 10.1210/endo.138.10.5446 · DOI
  8. 10.1111/j.1469-7793.1998.605bk.x · DOI
  9. 10.1210/endo-123-1-396 · DOI
  10. 10.1677/joe.0.1110027 · DOI
  11. 10.1210/endo.139.2.5721 · DOI · Paper page
  12. 10.1046/j.1365-2826.2001.00715.x · DOI
  13. 10.1073/pnas.86.12.4771 · DOI · Paper page
  14. 10.1126/science.156.3772.258 · DOI · Paper page
  15. 10.1210/en.2004-1201 · DOI
  16. 10.1113/jphysiol.2004.078212 · DOI
  17. Gardner KL, 2006, Early Life Experience Programs Gene Expression in Serotonin Neurons
  18. John S, 2008, Molecular Cell, 611

Cited by

Metadata

Authors
Lightman, S. L.
Venue
Journal of Neuroendocrinology
Publisher
Wiley
Published
2008-06
Volume
20
Issue
6
Pages
880-884
ISSN
  • 0953-8194 (ISSN-L)
  • 1365-2826
DOI
10.1111/j.1365-2826.2008.01711.x
OpenAlex
W2159202946
Cited by
3,566
References
24
FWCI
24.72
Type
journal article
Language
en
Open access
closed
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor, 39 d)

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