Induction of Fos-like protein in neurons of the medulla oblongata after electrical stimulation of the vagus nerve in anesthetized rabbit

1994 ◽  
Vol 635 (1-2) ◽  
pp. 317-322 ◽  
Author(s):  
M. Yousfi-Malki ◽  
J.J. Puizillout
Keyword(s):  
Electrical Stimulation ◽  
Vagus Nerve ◽  
Medulla Oblongata ◽  
Stimulation Of

Vasopressin secretion after stimulation of abdominal vagus in rabbit: role of A1 norepinephrine neurons

1994 ◽  
Vol 266 (6) ◽  
pp. R1885-R1890 ◽  
Author(s):  
Z. J. Gieroba ◽  
W. W. Blessing
Keyword(s):  
Electrical Stimulation ◽  
Vagus Nerve ◽  
Medulla Oblongata ◽  
Vagal Stimulation ◽  
Vagal Afferents ◽  
Neuronal Function ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
Stimulation Of

We determined whether electrical stimulation of the abdominal vagus nerve causes secretion of vasopressin in the rabbit and whether inhibition of neuronal function in the A1 region of the medulla oblongata impairs this secretion. In urethan-anesthetized rabbits, electrical stimulation of the abdominal vagus (5-min train of cathodal pulses, 0.5 ms duration, 20 Hz, 0.5-1 mA) increased plasma vasopressin from 37 +/- 8 to 133 +/- 19 pg/ml (P < 0.01, n = 11). Prior section of the cervical vagus completely prevented the increase seen with stimulation of the abdominal vagus. Injecting the inhibitory agent muscimol (1 nmol) 2 mm dorsal to the A1 area did not significantly reduce the vasopressin response to abdominal vagal stimulation. However, when muscimol was injected into the A1 area, the vagally mediated increase in plasma vasopressin was completely prevented. Our results show that stimulation of abdominal vagal afferents causes secretion of vasopressin in the rabbit via a central pathway that includes neurons in the A1 area.

Electrical Stimulation of the Vagus Nerve Modulates the Development of Oxygen Epilepsy in Rabbits

2017 ◽  
Vol 47 (3) ◽  
pp. 345-351
Author(s):  
S. Yu. Zhilyaev ◽  
A. N. Moskvin ◽  
T. F. Platonova ◽  
I. T. Demchenko
Keyword(s):  
Electrical Stimulation ◽  
Vagus Nerve ◽  
Stimulation Of

Hyperinsulinemia of preobese and obese fa/fa rats is partly vagus nerve mediated

1983 ◽  
Vol 244 (4) ◽  
pp. E317-E322 ◽  
Author(s):  
F. Rohner-Jeanrenaud ◽  
A. C. Hochstrasser ◽  
B. Jeanrenaud
Keyword(s):  
Electrical Stimulation ◽  
Insulin Secretion ◽  
B Cells ◽  
Vagus Nerve ◽  
Zucker Rats ◽  
Glucose Load ◽  
Parasympathetic System ◽  
Enhanced Sensitivity ◽  
Stimulation Of

In vivo glucose-induced insulin secretion was greater in preweaned preobese 17-day-old Zucker rats than in the corresponding controls. This hypersecretion of insulin was reversed to normal by acute pretreatment with atropine. A short-lived (30 s) electrical stimulation of the vagus nerve preceding a glucose load potentiated the in vivo glucose-induced insulin release in adult animals (6-9 wk) and more so in obese Zucker (fa/fa) than in lean rats. This suggested the existence of enhanced sensitivity and/or responsiveness of the B cells of obese animals to the parasympathetic system. That the parasympathetic tone was increased in adult obese Zucker (fa/fa) rats was corroborated by the observation that acute vagotomy of these animals resulted in a significant decrease in glucose-induced insulin secretion, whereas no such effect was seen in lean rats. Also, perfused pancreases from adult obese (fa/fa) rats oversecreted insulin during a stimulation by arginine when compared with controls, an oversecretion that was restored toward normal by superimposed infusion of atropine. It is concluded that a) the increased insulin secretion of preobese Zucker fa/fa rats is an early abnormality that is mediated by the vagus nerve, and b) increased secretion of insulin in adult obese fa/fa rats continues to be partly vagus-nerve mediated, although a decreased sympathetic tone and other unknown defects could conceivably play a role as well.

scholarly journals Effect of distal esophageal irritation on the changes of cystometry parameters to esophagus and colon distentions in rats

2019 ◽  
Vol 97 (8) ◽  
pp. 766-772
Author(s):  
Ezidin G. Kaddumi
Keyword(s):  
Electrical Stimulation ◽  
Urinary Bladder ◽  
Vagus Nerve ◽  
Storage Time ◽  
Distal Colon ◽  
Bladder Function ◽  
Maximum Pressure ◽  
Pressure Amplitude ◽  
Chemical Irritation ◽  
Stimulation Of

The coexistence of different visceral pathologies in patients suffering from irritable bowel syndrome, interstitial cystitis, and other pathologies, necessitates the study of these pathologies under complicated conditions. In the present study, cystometry recordings were used to investigate the effect of distal esophageal chemical irritation on the urinary bladder interaction with distal colon distention, distal esophageal distention, and electrical stimulation of abdominal branches of vagus nerve. Distal esophageal chemical irritation significantly decreased the intercontraction time via decreasing the voiding time. Also, distal esophageal chemical irritation significantly decreased the pressure amplitude by decreasing the maximum pressure. Following distal esophageal chemical irritation, distal esophageal distention was able to significantly decrease the intercontraction time by decreasing the storage time. However, 3 mL distal colon distention significantly increased the intercontraction time by increasing the storage time. On the other hand, following distal esophageal chemical irritation, electrical stimulation of abdominal branches of vagus nerve did not have any significant effect on intercontraction time. However, electrical stimulation of abdominal branches of vagus nerve significantly increased the pressure amplitude by increasing the maximum pressure. The results of this study demonstrate that urinary bladder function and interaction of bladder with other viscera can be affected by chemical irritation of distal esophagus.

The influence of electrical stimulation of vagus nerve on elemental composition of dopamine related brain structures in rats

2012 ◽  
Vol 61 (2) ◽  
pp. 156-165 ◽  
Author(s):  
Magdalena Szczerbowska-Boruchowska ◽  
Anna Krygowska-Wajs ◽  
Agata Ziomber ◽  
Piotr Thor ◽  
Pawel Wrobel ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Vagus Nerve ◽  
Elemental Composition ◽  
Brain Structures ◽  
Stimulation Of

Electrical stimulation of the vagus nerve modulates the histamine content of mast cells in the rat jejunal mucosa

Neuroreport ◽  
1995 ◽  
Vol 7 (1) ◽  
pp. 313-317 ◽  
Author(s):  
Thomas P. Gottwald ◽  
Bryan R. Hewlett ◽  
Sárka Lhoták ◽  
Ron H. Stead
Keyword(s):  
Electrical Stimulation ◽  
Mast Cells ◽  
Vagus Nerve ◽  
Histamine Content ◽  
Jejunal Mucosa ◽  
Stimulation Of

Localization of Spontaneous Respiratory Neuronal Activities in the Medulla Oblongata of the Cat: A New Location of the Expiratory Center

1957 ◽  
Vol 190 (2) ◽  
pp. 350-355 ◽  
Author(s):  
Edgar Haber ◽  
Kurt W. Kohn ◽  
S. H. Ngai ◽  
D. A. Holaday ◽  
S. C. Wang
Keyword(s):  
Vagus Nerve ◽  
Reticular Formation ◽  
Medulla Oblongata ◽  
Electric Stimulation ◽  
The Other ◽  
Drug Induced ◽  
Other Hand ◽  
Twin Beam ◽  
New Location ◽  
Stimulation Of

Medulla oblongata of 80 vagotomized cats was explored with microelectrodes. Spontaneous respiratory neuronal activities and chest movements were recorded simultaneously with a twin beam cathode ray oscilloscope. It was found that inspiratory discharges are concentrated in the reticular formation between 3 mm rostral and 1 mm caudal to the level of the obex, which corresponds approximately to the inspiratory region of Pitts, Magoun and Ranson. On the other hand, expiratory discharges are not obtained in Pitts' expiratory area, but are found in a circumscribed region in the reticular formation from the level of the obex to 3 mm caudally. Electric stimulation of this region has been found recently by Ngai and Wang to yield marked expiratory spasm. It is concluded that the expiratory center is located caudally to the inspiratory center in the cat. The spontaneous respiratory neuronal discharges continue with no alterations of pattern of firing during drug-induced respiratory paralysis, and are increased both in number and in frequency during CO2 inhalation. Stimulation of the vagus nerve with 50 shocks/sec. reduces inspiratory discharges and prolongs the duration of expiratory discharges.

Effects of calcium channel antagonists on the vagally mediated cardiac chronotropic response in dogs

1990 ◽  
Vol 68 (10) ◽  
pp. 1363-1367 ◽  
Author(s):  
Don W. Wallick ◽  
Sherry L. Stuesse ◽  
Paul Martin
Keyword(s):  
Electrical Stimulation ◽  
Vagus Nerve ◽  
Calcium Channel ◽  
Total Dose ◽  
Cycle Length ◽  
Cardiac Cycle ◽  
Vagal Stimulation ◽  
Calcium Channel Antagonists ◽  
Chronotropic Response ◽  
Stimulation Of

A brief electrical stimulation of the vagus nerve may elicit a triphasic response comprising (i) an initial prolongation of the same or the next cardiac cycle, (ii) a return of the subsequent cardiac cycle to about the level prior to vagal stimulation, and (iii) a secondary prolongation of cardiac cycle length that lasts several beats. We compared the effects of two calcium channel antagonists, verapamil and nifedipine, on this triphasic response to vagal stimulation in chloralose-anesthetized, open-chest dogs. In the absence of vagal stimulation, nifedipine (doses of 10, 40, and 50 μg/kg for a total dose of 100 μg/kg, i.v.) and verapamil (two doses of 100 μg/kg each, i.v.) increased the cardiac cycle length (A–A interval) by 16% (429 ± 20 to 496 ± 21 ms) and 29% (470 ± 33 to 605 ± 54 ms), respectively. Nifedipine (100 μg/kg total) attenuated the initial vagally mediated prolongation of the A–A interval, from 474 ± 19 to 369 ± 42 ms above the basal A–A interval. Following the initial prolongation of the vagal effect, other A–A intervals were not affected. In contrast, verapamil potentiated the vagally mediated initial prolongation in cardiac cycle length at the first dose administered (100 μg/kg) from 492 ± 17 to 561 ± 14 ms, but other increases in dosages had no further effect. Thus these two calcium channel antagonists have different effects on the sinoatrial chronotropic responses caused by brief vagal stimulation.Key words: autonomic control, parasympathetic, heart, calcium.

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