title: Corticosterone as a marker of susceptibility to oxidative/nitrosative cerebral damage after stress exposure in rats.
abstract: There are important individual differences in susceptibility to stress-induced diseases, most of them associated to the hypothalamic-pituitary and sympatho-medullo-adrenal axis functioning. Characterization of individual differences in animals may help to find the origin of this susceptibility. In order to study differences in oxidative and neuroinflammatory consequences in brain after stress exposure, we used an adult, male, outbred (Wistar:Hannover) population of 60 rats. Animals were subjected to 6h of immobilisation stress. Basal (1 week before stress) and post-stress (immediately after stress) plasma corticosterone (CC) was measured for each animal from the tail vein (basal: 239.74+/-19.44 ng/ml at 1500 h). Group H was assigned to animals with 33% higher levels of CC (>279.53 ng/ml) and group L to animals with 33% lower levels of CC (<199.09 ng/ml). After stress, animals with higher plasma CC levels in basal conditions showed higher adrenal response (higher post-stress CC levels) than rats with lower levels of basal CC. Furthermore, rats from H group are more vulnerable to accumulation of oxidative/nitrosative mediators in brain (higher calcium-independent nitric oxide activity and higher lipid peroxidation, by malondialdehyde determination, MDA) and also to the accumulation of proinflammatory mediators (higher PGE(2) levels) whereas showing less antiinflammatory protection (less 15-deoxy-PGJ(2) levels). Statistical analysis, by using ROC curves revealed cut-off values of basal plasma CC predicting animals with higher post-stress MDA and PGE(2) and lower PGJ(2) levels in brain. These data indicate that plasma basal levels of CC are an easily detectable and reproducible parameter for predicting the response of the individuals after an acute stress, providing further support for studies on individual differences.
authors.affiliation: Department of Pharmacology, Faculty of Medicine, University Complutense, Madrid 28040, Spain.
authors.forename: B G
authors.initials: BG
authors.lastname: Pérez-Nievas
authors.forename: B
authors.initials: B
authors.lastname: García-Bueno
authors.forename: J R
authors.initials: JR
authors.lastname: Caso
authors.forename: L
authors.initials: L
authors.lastname: Menchén
authors.forename: J C
authors.initials: JC
authors.lastname: Leza
mesh_terms: D000818:Animals; D021461:Animals, Outbred Strains; D015415:Biomarkers / Q000097:blood; D001921:Brain / Q000378:metabolism / Q000473:pathology; D001927:Brain Diseases / Q000097:blood / Q000139:chemically induced* / Q000473:pathology; D003345:Corticosterone / Q000097:blood*; D015232:Dinoprostone / Q000096:biosynthesis; D004198:Disease Susceptibility / Q000097:blood / Q000175:diagnosis*; D019746:Intramolecular Oxidoreductases / Q000378:metabolism; D008297:Male; D018384:Oxidative Stress / Q000502:physiology*; D000071876:Prostaglandin-E Synthases; D051381:Rats; D017208:Rats, Wistar; D026361:Reactive Nitrogen Species / Q000633:toxicity*; D013315:Stress, Psychological / Q000473:pathology*
chemical_list: D015415:Biomarkers; D026361:Reactive Nitrogen Species; D019746:Intramolecular Oxidoreductases; D000071876:Prostaglandin-E Synthases; D015232:Dinoprostone; D003345:Corticosterone