The Electrical Stimulation of the Bed Nucleus of the Stria Terminalis Causes Oxidative Stress in Skeletal Muscle of Rats

Author:

Karnia Mateusz Jakub12ORCID,Myslinska Dorota3,Dzik Katarzyna Patrycja12ORCID,Flis Damian Jozef4ORCID,Ciepielewski Ziemowit Maciej3,Podlacha Magdalena3,Kaczor Jan Jacek1ORCID

Affiliation:

1. Department of Neurobiology of Muscle, Faculty of Rehabilitation and Kinesiology, Gdansk University of Physical Education and Sport, Kazimierza Gorskiego 1, 80-336 Gdansk, Poland

2. Faculty of Physical Education, Gdansk University of Physical Education and Sport, Kazimierza Gorskiego 1, 80-336 Gdansk, Poland

3. Department of Animal and Human Physiology, Faculty of Biology, University of Gdansk, 80-308 Gdansk, Poland

4. Department of Bioenergetics and Nutrition, Faculty of Rehabilitation and Kinesiology, Gdansk University of Physical Education and Sport, Kazimierza Gorskiego 1, 80-336 Gdansk, Poland

Abstract

Recent studies indicate that activation of hypothalamus-pituitary-adrenocortical axis (HPA) plays the crucial role in stress response, while several lines of evidence mark the bed nucleus of the stria terminalis (BST) as a major mediator of the HPA axis responses to stress. The purpose of this study was to investigate the influence of the corticosterone flux induced by the electrical stimulation of BST on markers of free radical damage of lipids and proteins and antioxidant enzyme activity in skeletal muscle of rats. The male Wistar rats were used and assigned to one of three groups: sham-operated (SHM; n=6), two-week (ST2; n=6), and four-week stimulated (ST4; n=5) groups. Blood, soleus, and extensor digitorum longus muscles were collected. The chronic, 4-week electrical stimulation of the BST evokes increased plasma corticosterone concentration, which resulted in oxidative stress in skeletal muscles. We found higher level of lipid peroxidation markers, lower level of protein oxidation marker, and elevated antioxidant enzyme activity in both muscles. Our findings have also potential implication showing that reaction to the long-term “psychological stress” may lead to free radical damage of muscle.

Funder

Science Foundation for Young Scientist

Publisher

Hindawi Limited

Subject

Cell Biology,Aging,General Medicine,Biochemistry

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