In der vorliegenden prospektiven Pilotstudie wurden die Hypothesen überprüft, dass es durch die nicht-invasive aurikuläre Vagusnervstimulation, jedoch nicht durch eine Kontrollstimulation am Ohrläppchen (Innervationsgebiet des N. trigeminus) zu einer mittels NIRS messbaren Zunahme des regionalen zerebralen Blutflusses und damit der kortikalen Aktivität im Bereich des präfrontalen Kortex, zu einer Steigerung der Befindlichkeit und zu einer Verbesserung der Kognition kommt. Die Ergebnisse zeigten eine Deaktivierung im Bereich des präfrontalen Kortex, wobei keine signifikanten Unterschiede zwischen der Vagusnerv- und der Kontrollstimulation in allen drei Modulen (Hirnaktivierung, Kognition, Befindlichkeit) nachweisbar waren. / The aim of this pilot study was to investigate the effects of vagus nerve stimulation on brain activity, cognitive parameters and well-being compared to a sham-stimulation of the ear lobe. The results showed a decrease in frontal brain activation upon auricular vagus nerve stimulation as measured by NIRS. However, there was no statistically significant difference between aVNS and sham stimulation.

A B S T R A C T The purposes of this study were: (a) to compare the effect of gastric vagal stimulation on phrenic nerve activity during respiration and fictive vomiting, (b) to evaluate the modulatory effect of the central pattern generators (CPGs) for respiration and vomiting following peripheral inputs from gastric vagus. Decerebrate, paralyzed, and ventilated cats were used in this study. Vomiting was induced by electric stimulation of the gastric vagus or injection of emetic drugs (e.g. apomorphine). Fictive vomiting was identified by a characteristic series of synchronous bursts of phrenic nerves and abdominal nerves. During respiratory phase, the average duration of the phrenic nerve activity was 0.79 ¡Ó 0.07 second. The average duration of the phrenic cycles was 2.55 ¡Ó 0.13 second. Spectral analysis indicated that the phrenic activation had high frequency oscillation of 85~95 Hz. Gastric vagus stimulation (100 Hz, 300 mA) during respiratory phase lead to a deviation of the phrenic duration of -0.04 seconds. The duration of phrenic cycles was also decreased (reduced 0.25 seconds). The spectral distribution of the phrenic neurogram was also shifted during gastric vagal stimulation (dextral to 100~110 Hz). During vomiting phase, the average duration of the phrenic activity was 0.22 ¡Ó 0.03 seconds which was shorter than that during respiratory phase. The duration of the phrenic cycle during vomiting was 0.54 ¡Ó0.08 second. The major distribution of the power spectrum of the phrenic neurogram during vomiting was 100~120 Hz which is apparently higher than that during the respiratory phase. Gastric vagus stimulation during vomiting showed an averagely increased phrenic cycle (0.74 ¡Ó 0.05 seconds), and a shift of its spectral distribution (dextral to 120~150 Hz). These results suggest that vomiting and respiration were controlled by separate CPGs. Since the output of these two CPGs can be modified by a common peripheral signal such as stimulatary input signal from the gastric vagus, it is postulated that these two CPGs might be highly overlaped. Alternatively, they might be equipped with a single neural network while possessing two separate functions. Normally, this naural network will presume respiratory function, once properly stimulated, such as by injecting apomorphine or by chronic electric stimulation of gastric vagus, functions of this neural network, driving same set of motor fibers (diaphragm and abdominal muscles), will be shifted from respiratory control to vomiting phase control.

Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 5 uppsatser.

Thesis (M.S.)--University of Wisconsin--Madison, 1969. / eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Thesis (M.L.S.)--University of Toledo, 2006. / Typescript. "A thesis [submitted] as partial fulfillment of the requirements of the Master of Liberal Studies degree." Bibliography: leaves 57-59.

The vagus nerve is the principal pathway by which autonomic sensory information is carried from the periphery to the CNS where it influences the activity of a numerous structures including the locus coeruleus. Electrical stimulation of the vagus nerve has been demonstrated to enhance performance in a variety of memory tasks in both rats and humans and is used clinically for the control of epilepsy in humans. Electrical stimulation of the vagus nerve has also been shown to improve functional recovery following experimental brain injury in rats. The central hypothesis in these experiments is that vagus nerve stimulation exerts its beneficial effects by mediating the release of norepinephrine in the CNS. The results from Experiment I indicate that VNS results in increased extracellular NE concentration in the hippocampus at both the 0.5 and 1.0 mA stimulus intensities, and in the cortex at the 1.0 mA intensity. Increased concentrations of extracellular NE induced by VNS, regardless of structure, were transient, dissipating before the subsequent baseline recording period. Further, VNS-induced alterations in extracellular NE concentrations were observed bilaterally. Insult to the CNS by means of FPI resulted in long lasting depression of extracellular NE concentrations in the cortex of the injured controls and 1.0 mA VNS group that was partially attenuated 1.0 mA VNS. In the 0.5 mA VNS group NE concentrations remained above pre-injury levels for the majority of the post-FPI measurement period. In the hippocampus, mean NE concentrations in the period immediately following FPI were decreased in comparison to pre-FPI concentrations. Concentrations of hippocampal NE remained depressed in the injured control group throughout the 48 hr sample period. Hippocampal NE concentrations in both the 0.5 mA VNS and 1.0 mA VNS group recovered to above pre-injury levels by 14-20 hrs post-FPI and were significantly higher than that of the injured controls in the 20-26 and 26-32 hr post-FPI sampling periods. Further, hippocampal NE concentrations remained significantly higher in 0.5 mA VNS group in comparison to injured controls in the 32-38 and 38-44 hr sampling periods.

Vagal afferents in the gut are polymodal for a multitude of chemical mediators, including beneficial and noxious sensory stimuli, and therefore must encode sensory information for the brain about the luminal environment. This sensory information has profound influence on related reflex pathways, gut function, and mood and behaviour via the gut-brain axis. Using an established mesenteric nerve recording protocol, we investigated how vagal afferents from the small intestine signal and encode information about luminal stimuli and somatic age to the brain. We investigated the role of an intramural sensory synapse between intrinsic primary afferent neurons (IPANs) of the enteric nervous system (ENS) and extrinsic vagal afferents in the gut wall in the excitatory response to luminal application of the vagus-dependent selective serotonin reuptake inhibitor (SSRI) sertraline. Vagal afferent excitation by sertraline was inhibited by intramural sensory synaptic blockade, indicating a potential role of IPAN to vagal crosstalk in the vagal response to sertraline. We examined patterns of vagal afferent firing produced by stimuli with opposing effects on behaviour to determine how the vagus encodes information pertaining to antidepressant stimuli. A distinct temporal pattern code of antidepressant vagal afferent signaling was identified that was different from the pattern code produced by non- antidepressant stimuli. Lastly, we examined how vagal afferent signaling to the brain differed in aged mice and in an aged Parkinson’s disease (PD) model. There was a significant reduction in vagal afferent firing in old and PD model mice, but this reduction was partially reversed by treatment with the excitatory aminosterol squalamine. These studies demonstrate that vagal afferent firing is critical to the communication of sensory information from the gut lumen to the brain and that this information is encoded in specific patterns of firing that are influenced by the type of stimulus and the welfare of the signalling pathway. / Thesis / Candidate in Philosophy / The vagus nerve connects the brain and gut enabling the transfer of bidirectional nervous signals, of which 80-90% transmit towards the brain. Some of these vagal signals that travel from the gut to the brain can modify behaviour or mood. We investigated a potential mechanism by which vagal afferents change firing in response to stimuli inside the gut to communicate mood-altering information to the brain and explored whether vagal signaling is vulnerable to aging. We presented evidence that the antidepressant sertraline increased vagal firing by synaptic signaling between neurons in the gut wall and vagal afferents. We demonstrated that antidepressant agents produced a specific pattern of action potential firing that might encode mood-altering information to the brain. Lastly, we found that aging and Parkinson’s disease decreased vagal afferent firing, but not insurmountably. This work identifies novel mechanisms by which intestinal vagal afferents signal the brain, which may have therapeutic applications.

No description available.

Thesis (Ph. D.)--Memorial University of Newfoundland, Faculty of Medicne, 2001. / Typescript. Includes bibliographical references (leaves 156-172).

Non-invasive transcutaneous auricular vagus nerve stimulation (taVNS) is a neuromodulatory technique used to activate vagal afferent fibers located in the concha of the outer ear. Vagal afferents project to the nucleus of the solitary tract (NTS) where information is processed and propagated to higher brain regions. Widespread NTS connections provide a mechanism through which taVNS can be used to influence multiple systems and be a potential treatment for many disorders including heart failure, gastric motility disorders, and migraines. Recent studies are now investigating taVNS as an alternative treatment option to invasive cervical vagus nerve stimulation (cVNS) which is FDA approved to treat drug-resistant epilepsy and depression but has limited patient availability due to the invasiveness of the procedure. Migraine and epilepsy clinical studies have shown therapeutic taVNS benefits and human fMRI studies have demonstrated comparable brain activation between cVNS and taVNS. However, questions remain regarding optimal taVNS parameters, and no study has compared the direct mechanisms responsible for cVNS and taVNS effects. In this study, a high-impedance tungsten electrode was stereotaxically placed into NTS in 10 chloralose-anesthetized rats, and 40-70 neurons were interrogated using electrophysiological methods. Firing rate changes during stimulation on-times were compared to activity levels during stimulation off-times. Neurons were classified as positive responders if they displayed consistent firing rate increases during stimulation, negative responders if they displayed consistent decreases, and non-responders if there was no consistency using a mathematical cosine similarity score. Six taVNS stimulation parameters were investigated using three frequencies (20, 100, 250Hz) at two intensities (0.5, 1.0mA) to identify parameter-specific effects on NTS neurons. Additionally, neuronal activity was evaluated following cVNS at 20 and 250Hz at the bradycardic intensity (lowest intensity to generate a transient 5% decrease in heart rate, BI) and compared to taVNS effects at the corresponding frequencies. Our data shows that taVNS at 20Hz, 1.0mA yields the greatest number of positive responders and 100Hz, 1.0mA yields the greatest number of negative responders (p<0.05) suggesting different taVNS parameters can differentially influence NTS activity. Comparisons between the number of responders generated with cVNS and taVNS revealed significantly fewer negative responders with cVNS at 20Hz compared to taVNS at 20Hz regardless of intensity (p<0.01) but yielded comparable positive responders between cVNS at 20Hz, BI and taVNS at 20Hz, 1.0mA. No significant differences were observed between the number of cVNS and taVNS responders at 250Hz. Interestingly, individual neuronal responses were different between both methods of stimulation, suggesting that they could work through different neuronal pathways.