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Chronic stress decreases the expression of sympathetic markers in the pineal gland and increases plasma melatonin concentration in rats.

Authors :
Dagnino-Subiabre, Alexies
Orellana, Juan A.
Carmona-Fontaine, Carlos
Montiel, Juan
Díaz-Velíz, Gabriela
Serón-Ferr, María
Wyneken, Ursula
Concha, Miguel L.
Aboitiz, Francisco
Source :
Journal of Neurochemistry; Jun2006, Vol. 97 Issue 5, p1279-1287, 9p, 2 Color Photographs, 1 Black and White Photograph, 4 Graphs
Publication Year :
2006

Abstract

Chronic stress affects brain areas involved in learning and emotional responses. Although most studies have concentrated on the effect of stress on limbic-related brain structures, in this study we investigated whether chronic stress might induce impairments in diencephalic structures associated with limbic components of the stress response. Specifically, we analyzed the effect of chronic immobilization stress on the expression of sympathetic markers in the rat epithalamic pineal gland by immunohistochemistry and western blot, whereas the plasma melatonin concentration was determined by radioimmunoassay. We found that chronic stress decreased the expression of three sympathetic markers in the pineal gland, tyrosine hydroxylase, the p75 neurotrophin receptor and α-tubulin, while the same treatment did not affect the expression of the non-specific sympathetic markers Erk1 and Erk2, and glyceraldehyde-3-phosphate dehydrogenase. Furthermore, these results were correlated with a significant increase in plasma melatonin concentration in stressed rats when compared with control animals. Our findings indicate that stress may impair pineal sympathetic inputs, leading to an abnormal melatonin release that may contribute to environmental maladaptation. In addition, we propose that the pineal gland is a target of glucocorticoid damage during stress. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
00223042
Volume :
97
Issue :
5
Database :
Complementary Index
Journal :
Journal of Neurochemistry
Publication Type :
Academic Journal
Accession number :
20791347
Full Text :
https://doi.org/10.1111/j.1471-4159.2006.03787.x