Cardiovascular responses to electrical stimulation of the bed nucleus of the stria terminalis

1995 ◽  
Vol 352 (2) ◽  
pp. 227-234 ◽  
Author(s):  
J.D. Dunn ◽  
T.J. Williams
Keyword(s):  
Electrical Stimulation ◽  
Cardiovascular Responses ◽  
Stria Terminalis ◽  
Bed Nucleus ◽  
Stimulation Of

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

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Mateusz Jakub Karnia ◽  
Dorota Myslinska ◽  
Katarzyna Patrycja Dzik ◽  
Damian Jozef Flis ◽  
Ziemowit Maciej Ciepielewski ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Enzyme Activity ◽  
Electrical Stimulation ◽  
Antioxidant Enzyme Activity ◽  
Stria Terminalis ◽  
Free Radical Damage ◽  
Bed Nucleus ◽  
Radical Damage ◽  
Stimulation Of

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.

scholarly journals Electrical stimulation of the bed nucleus of the stria terminalis reduces anxiety in a rat model

2017 ◽  
Vol 7 (2) ◽  
pp. e1033-e1033 ◽  
Author(s):  
K Luyck ◽  
T Tambuyzer ◽  
M Deprez ◽  
J Rangarajan ◽  
B Nuttin ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Rat Model ◽  
Stria Terminalis ◽  
Bed Nucleus ◽  
Stimulation Of

Long-term electrical stimulation of bed nucleus of stria terminalis for obsessive-compulsive disorder

2016 ◽  
Vol 22 (6) ◽  
pp. 931-934 ◽  
Author(s):  
S Raymaekers ◽  
K Vansteelandt ◽  
L Luyten ◽  
C Bervoets ◽  
K Demyttenaere ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Obsessive Compulsive Disorder ◽  
Stria Terminalis ◽  
Obsessive Compulsive ◽  
Bed Nucleus ◽  
Compulsive Disorder ◽  
Stimulation Of

Effect of glutamate stimulation of bed nucleus of the stria terminalis on arterial pressure and heart rate

1993 ◽  
Vol 265 (5) ◽  
pp. H1516-H1522 ◽  
Author(s):  
J. Ciriello ◽  
S. A. Janssen
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Excitatory Amino Acid ◽  
Anterior Commissure ◽  
Cardiovascular Responses ◽  
Receptor Blocker ◽  
Stria Terminalis ◽  
Bed Nucleus ◽  
Stimulation Of

Experiments were done in the chloralose-anesthetized, paralyzed, and artificially ventilated rat to determine the cardiovascular responses elicited during chemical stimulation of bed nucleus of the stria terminalis (BST) and to investigate the components of the peripheral autonomic nervous system that mediate these responses. Neurons in BST were selectively stimulated by the microinjection (10-20 nl) of the excitatory amino acid L-glutamate (1 M). Stimulation of BST elicited decreases in mean arterial pressure (n = 105) of -6 to -55 mmHg. These depressor responses were on occasion (n = 60) accompanied by decreases in heart rate ranging between -10 and -40 beats/min. The largest depressor responses were consistently elicited from a crescent-shaped region of BST around the dorsolateral, lateral, and ventrolateral surfaces of the anterior commissure. Intravenous administration of the muscarinic receptor blocker, atropine methylbromide, had no affect on the magnitude of the mean arterial pressure and heart rate responses. On the other hand, administration (intravenous) of the nicotinic receptor blocker, hexamethonium bromide or arfonad, abolished both the depressor response and cardiac slowing during stimulation of BST. These data suggest that the BST depressor and the bradycardia responses are mediated by inhibition of both sympathetic vasoconstrictor fibers to the vasculature and cardioacceleratory fibers to the heart, respectively.

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