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

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.

BST Stimulation Induces Atrophy and Changes in Aerobic Energy Metabolism in Rat Skeletal Muscles—The Biphasic Action of Endogenous Glucocorticoids

“…It implies a conviction that a white muscle is more susceptible to develop adverse effects of GCs action. Our observation of a higher level of protein oxidation in EDL, as compared to SOL muscle, in the CSR rats partially proves previous results [17]. On the other hand, our results show that in EDL, not GR but MR content is dominant, and could be a significant contributing factor in muscle devastation.…”

“…Lately, we demonstrated on the same experimental model that rats' plasma CORT level after the BST stimulation significantly increased in the four weeks stimulated group (ST4) group as compared with the two weeks stimulated (ST2) and sham-stimulated (SHM) groups [17]. The results are summarized in Table 1.…”

“…According to our knowledge, this is the first preclinical work that shows the interplay between HSD11B (type 1 and 2) and GR/MR in the CSR conditions. Obtained data show that the CSR linked with the elevated CORT level [17] inducing the skeletal muscle atrophy is associated with the FOXO/atrogin-1 pathway. Our observations confirm the previously published data, which clearly shows that HSD11B1 may be a major regulator of the muscular atrophy.…”

“…In our recent work, it was presented that the CSR induced by the electrical stimulation of the BST causes the elevated level of markers lipid and protein peroxidation in EDL muscle. However, no changes in protein oxidation but only the higher level of lipid peroxidation marker in the SOL muscle was found [17]. Furthermore, the oxidation of sulfhydryl groups likely contributes to the deactivation and degradation of mitochondrial enzymes and transport proteins [27].…”

“…The animals used in the experiment were previously described by Karnia and co-workers [17]. Briefly, male Wistar rats (n = 17) weighing 250-300 g were used.…”