Respiratory periodicity following stimulation of vagal afferents

1980 ◽  
Vol 58 (7) ◽  
pp. 823-829 ◽  
Author(s):  
Steve Iscoe ◽  
Stephen Vanner

The effects on respiratory periodicity of electrical stimulation of the cut central end of a vagus nerve were studied in anaesthetized, vagotomized, paralyzed, and ventilated rabbits. Electrical activity of a phrenic nerve was used to determine inspiratory and expiratory durations (Ti and Te). The central cut end of one vagus nerve was electrically stimulated during the entire inspiratory phase of every 10th respiratory cycle and Ti and Te of that respiratory cycle and the following 8 were measured. When only the fastest conducting afferents (pulmonary stretch receptor afferents) were stimulated, reductions in Ti and Te were restricted to the stimulated cycle. When stimulus intensity was increased, activating higher threshold, more slowly conducting afferents (including those of irritant receptors), Te but not necessarily Ti decreased, increasing the frequency of phrenic bursts (respiratory frequency). The recovery of Te following stimulation was exponential, with a time constant of 3–7 s which varied inversely with control respiratory frequency. The effects on Ti and Te on higher intensity stimulation suggest either that coupling between inspiratory and expiratory neurones in the brainstem respiratory oscillator can be "looser" than currently hypothesized or a separate population of expiratory neurones, with a short-term memory (three time constants or [Formula: see text]), mediates the observed effects.

2019 ◽  
Author(s):  
Vanessa Teckentrup ◽  
Sandra Neubert ◽  
João C. P. Santiago ◽  
Manfred Hallschmid ◽  
Martin Walter ◽  
...  

AbstractMetabolic feedback between the gut and the brain relayed via the vagus nerve contributes to energy homeostasis. We investigated in healthy adults whether non-invasive stimulation of vagal afferents impacts energy homeostasis via efferent effects on metabolism or digestion. In a randomized crossover design, we applied transcutaneous auricular vagus nerve stimulation (taVNS) while recording efferent metabolic effects using simultaneous electrogastrography (EGG) and indirect calorimetry. We found that taVNS reduced gastric myoelectric frequency (p =.008), but did not alter resting energy expenditure. We conclude that stimulating vagal afferents induces gastric slowing via vagal efferents without acutely affecting net energy expenditure at rest. Collectively, this highlights the potential of taVNS to modulate digestion by activating the dorsal vagal complex. Thus, taVNS-induced changes in gastric frequency are an important peripheral marker of brain stimulation effects.


2006 ◽  
Vol 24 (4) ◽  
pp. 164-168 ◽  
Author(s):  
Yusuf Ozgur Cakmak

Vagal nerve stimulation and electroacupuncture have some promise as neuroprotective therapies for patients with poorly controlled epilepsy. It has been demonstrated that stimulation of acupuncture points on the extremities results in stimulation of the vagus nerve. It is possible that the antiepileptic effects of these two applications might be targeting the same centre in the brain. The nucleus of the solitary tract, which is a primary site at which vagal afferents terminate, is also the site for afferent pathways of facial, scalp and auricular acupuncture via trigeminal, cervical spinal and glossopharyngeal nerves. Taken together with laboratory findings, the neuroprotective pathways of electroacupuncture in epileptic models may stem from the collaboration of its anti-inflammatory and neurotrophic actions through the nucleus of the solitary tract via vagus nerve stimulation.


2021 ◽  
Author(s):  
Jonathan A. Shulgach ◽  
Dylan W. Beam ◽  
Ameya C. Nanivadekar ◽  
Derek M. Miller ◽  
Stephanie Fulton ◽  
...  

AbstractDysfunction and diseases of the gastrointestinal (GI) tract are a major driver of medical care. The vagus nerve innervates and controls multiple organs of the GI tract and vagus nerve stimulation (VNS) could provide a means for affecting GI function and treating disease. However, the vagus nerve also innervates many other organs throughout the body, and off-target effects of VNS could cause major side effects such as changes in blood pressure. In this study, we aimed to achieve selective stimulation of populations of vagal afferents using a multi-contact cuff electrode wrapped around the abdominal trunks of the vagus nerve. Four-contact nerve cuff electrodes were implanted around the dorsal (N=3) or ventral (N=3) abdominal vagus nerve in six ferrets, and the response to stimulation was measured via a 32-channel microelectrode array (MEA) inserted into the nodose ganglion. Selectivity was characterized by the ability to evoke responses in MEA channels through one bipolar pair of cuff contacts but not through the other bipolar pair. We demonstrated that is was possible to selectively activate subpopulations of vagal afferents using abdominal VNS. Additionally, we quantified the conduction velocity of evoked responses to determine what types of nerve fibers (i.e. Aδ vs. C) responded to stimulation. We also quantified the spatial organization of evoked responses in the nodose MEA to determine if there is somatotopic organization of the neurons in that ganglion. Finally, we demonstrated in a separate set of three ferrets that stimulation of the abdominal vagus via a four-contact cuff could selectively alter gastric myoelectric activity, suggesting that abdominal VNS can potentially be used to control GI function.


1994 ◽  
Vol 266 (6) ◽  
pp. R1885-R1890 ◽  
Author(s):  
Z. J. Gieroba ◽  
W. W. Blessing

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.


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