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Article type: Short Communication
Authors: Lejavova, Katarinaa; b | Ondicova, Katarinaa; b | Horvathova, Lubicaa | Hegedusova, Noemib | Cubinkova, Veronikac | Vargovic, Petera | Manz, Georgd | Filipcik, Peterc | Mravec, Borisa; b | Novak, Michalc | Kvetnansky, Richarda; *
Affiliations: [a] Institute of Experimental Endocrinology, Slovak Academy of Sciences, Bratislava, Slovak Republic | [b] Faculty of Medicine, Comenius University, Bratislava, Slovak Republic | [c] Institute of Neuroimmunology, Slovak Academy of Sciences, Bratislava, Slovak Republic | [d] Labor Diagnostika Nord, Nordhorn, Germany
Correspondence: [*] Correspondence to: Richard Kvetnansky, DSc, Institute of Experimental Endocrinology, Slovak Academy of Sciences, Vlarska 3, 833 06 Bratislava, Slovak Republic. Tel.: +421 2 54772709; Fax: +421 2 54774908; E-mail: ueenkvet@savba.sk.
Abstract: Stress may accelerate onset of neurodegenerative diseases in vulnerable subjects and, vice versa, neurodegeneration affects the responsiveness to stressors. We investigated the neuroendocrine response to immobilization stress in normotensive Wistar-Kyoto rats (WKY), spontaneously hypertensive rats (SHR), and transgenic rats of respective WKY and SHR strains overexpressing human truncated tau protein. Plasma levels of epinephrine, norepinephrine, and corticosterone were determined. An immobilization-induced elevation of epinephrine and norepinephrine was significantly reduced in WKY transgenic rats compared to WKY wild-type rats, while no differences were seen between SHR transgenic and SHR wild-type animals. Our data have shown that sympathoadrenal system response to stress strongly depends on both tau protein-induced neurodegeneration and genetic background of experimental animals.
Keywords: Alzheimer's disease, corticosterone, epinephrine, hypothalamic-pituitary adrenocortical axis, norepinephrine, stress, sympathoadrenal system, tauopathy
DOI: 10.3233/JAD-141329
Journal: Journal of Alzheimer's Disease, vol. 43, no. 4, pp. 1157-1161, 2015
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