Repeated (isolation) stress increases tribulin-like activity in the rat
Document Type
Journal Article
Publication Date
3-1-1989
Journal
Cellular and Molecular Neurobiology
Volume
9
Issue
1
DOI
10.1007/BF00711448
Keywords
benzodiazepine receptor binding inhibitory activity; isolation stress; monoamine oxidase (MAO) inhibitory activity; plasma catecholamines; repeated stress; tribulin
Abstract
1. The effect of repeated isolation stress on MAO inhibitory activity (tribulin) in rat tissues as well as on plasma catecholamine levels was invstigated. 2. Animals were subjected to a daily period of isolation (9min) and sacrificed on days 1, 2, 4, and 5. 3. In brain and cerebellum the levels of both inhibitory activities were found to be significantly higher in animals sacrificed on days 1-2 than in either controls or animals sacrificed on days 4-5. 4. In heart and kidney the highest levels of both activities were found in animals sacrificed on days 4-5. 5. Plasma levels of dopamine on day 4 were significantly higher than those in controls or in any of the experimental groups. Plasma levels of epinephrine showed step-by-step increments from day 1 up to day 5, reaching statistical significance only on day 5. Plasma levels of norepinephrine were significantly increased on days 2, 4, and 5. 6. Under the experimental conditions of this study, we have shown a rapid and short-lasting increment of tribulin in the central nervous system. Its disappearance on days 4-5 could be related to adaptation to the novel situation. Changes in the peripheral tissues appeared later, and a similar adaptation was absent during the period of observation. 7. Tribulin would be related to the stressful situation not only as an anxiety-promoting agent but also in contributing to the maintenance of high levels of circulating catecholamines. © 1989 Plenum Publishing Corporation.
APA Citation
Armando, I., Lemoine, A., Ferrini, M., Segura, E., & Barontini, M. (1989). Repeated (isolation) stress increases tribulin-like activity in the rat. Cellular and Molecular Neurobiology, 9 (1). http://dx.doi.org/10.1007/BF00711448