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1
Champeil-Potokar, G., O. Rampin, A. M. Davila, et al. "Plasticité gliale dans le complexe dorso-vagal en réponse à des régimes « gras-sucrés » de type occidental." Nutrition Clinique et Métabolisme 35, no. 1 (2021): 35. http://dx.doi.org/10.1016/j.nupar.2021.01.033.
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Caspar, V., T. Charleux, A. Beddok, et al. "Impact dosimétrique de la dose au complexe vagal dorsal et survenue de nausées en cours de radiothérapie." Cancer/Radiothérapie 25, no. 6-7 (2021): 734–35. http://dx.doi.org/10.1016/j.canrad.2021.07.018.
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Champeil-Potokar, G., L. Jaulin, M. S. Hjeij, A. Couvineau, A. Blais, and I. Denis. "Effets d’un régime gras-sucré (GS) et d’un traitement aux orexines A (OxA) sur la plasticité gliale dans le complexe dorso-vagal chez la souris." Nutrition Clinique et Métabolisme 36, no. 1 (2022): S13. http://dx.doi.org/10.1016/j.nupar.2021.12.024.
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Okumura, T., I. L. Taylor, and T. N. Pappas. "Microinjection of TRH analogue into the dorsal vagal complex stimulates pancreatic secretion in rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 269, no. 3 (1995): G328—G334. http://dx.doi.org/10.1152/ajpgi.1995.269.3.g328.
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Thyrotropin-releasing hormone (TRH) stimulates pancreatic exocrine secretion through the vagus nerve when injected into rat cerebrospinal fluid. However, little is known about the exact site of action of TRH in the brain to stimulate pancreatic secretion. Recent neuroimmunochemical and neurophysiological studies suggest that TRH could be a neurotransmitter in the dorsal vagal complex, which sends fibers to the pancreas through the vagus nerve. We therefore hypothesized that TRH may act centrally in the dorsal vagal complex to stimulate pancreatic exocrine secretion. To address this question, a TRH analogue, [1-methyl-(S)-4,5-dihydroorotyl]-L-histidyl-L-prolinamide- NH2, was microinjected into the dorsal vagal complex, and basal pancreatic fluid flow and protein secretion were measured in urethan-anesthetized rats. Microinjection of TRH analogue (0.2-2 ng/site) into the dorsal vagal complex significantly stimulated pancreatic flow and protein output in a dose-dependent manner. As a control, microinjection of the TRH analogue into the brain stem outside the vagal complex failed to stimulate pancreatic secretion. Either bilateral subdiaphragmatic vagotomy or atropine abolished the ability of the TRH analogue to stimulate pancreatic secretion. Our data suggest that TRH acts in the dorsal vagal complex to stimulate pancreatic secretion through vagus-dependent and cholinergic pathways. The dorsal vagal complex may play an important role as a central site for control of the exocrine pancreas.
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Viard, Eddy, Zhongling Zheng, Shuxia Wan, and R. Alberto Travagli. "Vagally mediated, nonparacrine effects of cholecystokinin-8s on rat pancreatic exocrine secretion." American Journal of Physiology-Gastrointestinal and Liver Physiology 293, no. 2 (2007): G493—G500. http://dx.doi.org/10.1152/ajpgi.00118.2007.
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Cholecystokinin (CCK) has been proposed to act in a vagally dependent manner to increase pancreatic exocrine secretion via actions exclusively at peripheral vagal afferent fibers. Recent evidence, however, suggests the CCK-8s may also affect brain stem structures directly. We used an in vivo preparation with the aims of 1) investigating whether the actions of intraduodenal casein perfusion to increase pancreatic protein secretion also involved direct actions of CCK at the level of the brain stem and, if so, 2) determining whether, in the absence of vagal afferent inputs, CCK-8s applied to the dorsal vagal complex (DVC) can also modulate pancreatic exocrine secretion (PES). Sprague-Dawley rats (250–400 g) were anesthetized and the common bile-pancreatic duct was cannulated to collect PES. Both vagal deafferentation and pretreatment with the CCK-A antagonist lorglumide on the floor of the fourth ventricle decreased the casein-induced increase in PES output. CCK-8s microinjection (450 pmol) in the DVC significantly increased PES; the increase was larger when CCK-8s was injected in the left side of the DVC. Protein secretion returned to baseline levels within 30 min. Microinjection of CCK-8s increased PES (although to a lower extent) also in rats that underwent complete vagal deafferentation. These data indicate that, as well as activating peripheral vagal afferents, CCK-8s increases pancreatic exocrine secretion via an action in the DVC. Our data suggest that the CCK-8s-induced increases in PES are due mainly to a paracrine effect of CCK; however, a relevant portion of the effects of CCK is due also to an effect of the peptide on brain stem vagal circuits.
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Wang, Sheng-Zhi, Xiao-Dong Liu, Yu-Xin Huang, Qing-Jiu Ma, and Jing-Jie Wang. "Disruption of Glial Function Regulates the Effects of Electro-Acupuncture at Tsusanli on Gastric Activity in Rats." American Journal of Chinese Medicine 37, no. 04 (2009): 647–56. http://dx.doi.org/10.1142/s0192415x09007132.
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According to recent evidence, acupuncture at Tsusanli (ST 36) can regulate gastric activity. And this regulation mainly depends upon neural basis or structure and may probably relate to the central neurons in the dorsal vagal complex. However, whether the glias of the dorsal vagal complex participate in the regulation of gastric activity, when electro-acupuncture (EA) at Tsusanli, still remains to be interpreted. In this study, we observed the effect of EA at Tsusanli (ST 36) on regulation of gastric activity. Propentofylline (PPF), a glial metabolic inhibitor, was used to inhibit the function of glial cells. EA at Tsusanli showed that the expressions of glial fibrillary acidic protein (GFAP) and OX42 increased significantly compared to that of the control group, and gastric electric change was obvious, with significantly higher frequency and wave amplitude compared to the control group. The expressions of GFAP and OX42 were decreased markedly when pretreated with PPF group than without PPF pretreatment group. Compared to the Tsusanli group and the control group, the changes of electro gastric graph (EGG) were significantly decreased in PPF pretreatment group. On the other hand, we observed the changes of spontaneous electro-activity of the DVC (dorsal vagal complex) in our previous experiment. The results indicated that EA at Tsusanli could activate glial cells in the dorsal vagal complex and regulate gastric activity. PPF blocked the function of glia, thus the effect of EA at Tsusanli on gastric activity was weakened. Our study suggested that this electro-acupuncture regulation of gastric activity was possibly related with glia of the dorsal vagal complex.
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Hornby, Pamela J. "II. Excitatory amino acid receptors in the brain-gut axis." American Journal of Physiology-Gastrointestinal and Liver Physiology 280, no. 6 (2001): G1055—G1060. http://dx.doi.org/10.1152/ajpgi.2001.280.6.g1055.
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In the last decade, there has been a dramatic increase in academic and pharmaceutical interest in central integration of vago-vagal reflexes controlling the gastrointestinal tract. Associated with this, there have been substantial efforts to determine the receptor-mediated events in the dorsal vagal complex that underlie the physiological responses to distension or variations in the composition of the gut contents. Strong evidence supports the idea that glutamate is a transmitter in afferent vagal fibers conveying information from the gut to the brain, and the implications of this are discussed in this themes article. Furthermore, both ionotropic and metabotropic glutamate receptors mediate pre- and postsynaptic control of glutamate transmission related to several reflexes, including swallowing motor pattern generation, gastric accommodation, and emesis. The emphasis of this themes article is on the potential therapeutic benefits afforded by modulation of these receptors at the site of the dorsal vagal complex.
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Powley, Terry L. "Brain-gut communication: vagovagal reflexes interconnect the two “brains”." American Journal of Physiology-Gastrointestinal and Liver Physiology 321, no. 5 (2021): G576—G587. http://dx.doi.org/10.1152/ajpgi.00214.2021.
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The gastrointestinal tract has its own “brain,” the enteric nervous system or ENS, that executes routine housekeeping functions of digestion. The dorsal vagal complex in the central nervous system (CNS) brainstem, however, organizes vagovagal reflexes and establishes interconnections between the entire neuroaxis of the CNS and the gut. Thus, the dorsal vagal complex links the “CNS brain” to the “ENS brain.” This brain-gut connectome provides reflex adjustments that optimize digestion and assimilation of nutrients and fluid. Vagovagal circuitry also generates the plasticity and adaptability needed to maintain homeostasis to coordinate among organs and to react to environmental situations. Arguably, this dynamic flexibility provided by the vagal circuitry may, in some circumstances, lead to or complicate maladaptive disorders.
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Powley, Terry L., and Robert J. Phillips. "I. Morphology and topography of vagal afferents innervating the GI tract." American Journal of Physiology-Gastrointestinal and Liver Physiology 283, no. 6 (2002): G1217—G1225. http://dx.doi.org/10.1152/ajpgi.00249.2002.
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An understanding of the events initiating vago-vagal reflexes requires knowledge of mechanisms of transduction by vagal afferents. Such information presumes an understanding of receptor morphology and location. Anatomic studies have recently characterized two types of vagal afferents, both putative mechanoreceptors distributed in gastrointestinal (GI) smooth muscle. These two receptors are highly specialized in that they 1) are morphologically distinct, 2) have different smooth muscle targets, 3) form complexes with dissimilar accessory cells, and 4) vary in their regional distributions throughout the GI tract. By comparison, information on the architecture and regional distributions of other classes of vagal afferents, notably chemoreceptors, has only begun to accumulate. Progress on the study of the two mechanoreceptors, however, illustrates general principles and delineates experimental issues that may apply to other submodalities of vagal afferents. By extension from morphological and physiological observations on the two species of smooth muscle endings, it is reasonable to hypothesize that additional classes of vagal receptors are also differentiated morphologically and that they vary in structure, accessory cells, regional distributions, and other features. A full appreciation of vago-vagal reflexes will require thorough structural and regional analyses of each of the types of vagal receptors within the GI tract.
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Rusetsky, I. I. "0 trigemino-vagal reflex." Kazan medical journal 18, no. 2 (2021): 84–104. http://dx.doi.org/10.17816/kazmj79881.
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Reflexology is the most fruitful part of neurology. With the accumulation of data in this area and the establishment of new principles and laws, our knowledge about the functions of the brain deepens, starting with simple reflexes of the medullae spinalis (Marschal ) and ending with complex reflexes of the cerebral hemispheres (combined, inhibited reflexes).
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Chen, S. L., X. Y. Wu, Z. J. Cao, et al. "Subdiaphragmatic vagal afferent nerves modulate visceral pain." American Journal of Physiology-Gastrointestinal and Liver Physiology 294, no. 6 (2008): G1441—G1449. http://dx.doi.org/10.1152/ajpgi.00588.2007.
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Activation of the vagal afferents by noxious gastrointestinal stimuli suggests that vagal afferents may play a complex role in visceral pain processes. The contribution of the vagus nerve to visceral pain remains unresolved. Previous studies reported that patients following chronic vagotomy have lower pain thresholds. The patient with irritable bowel syndrome has been shown alteration of vagal function. We hypothesize that vagal afferent nerves modulate visceral pain. Visceromotor responses (VMR) to graded colorectal distension (CRD) were recorded from the abdominal muscles in conscious rats. Chronic subdiaphragmatic vagus nerve sections induced 470, 106, 51, and 54% increases in VMR to CRD at 20, 40, 60 and 80 mmHg, respectively. Similarly, at light level of anesthesia, topical application of lidocaine to the subdiaphragmatic vagus nerve in rats increased VMR to CRD. Vagal afferent neuronal responses to low or high-intensity electrical vagal stimulation (EVS) of vagal afferent Aδ or C fibers were distinguished by calculating their conduction velocity. Low-intensity EVS of Aδ fibers (40 μA, 20 Hz, 0.5 ms for 30 s) reduced VMR to CRD at 40, 60, and 80 mmHg by 41, 52, and 58%, respectively. In contrast, high-intensity EVS of C fibers (400 μA, 1 Hz, 0.5 ms for 30 s) had no effect on VMR to CRD. In conclusion, we demonstrated that vagal afferent nerves modulate visceral pain. Low-intensity EVS that activates vagal afferent Aδ fibers reduced visceral pain. Thus EVS may potentially have a role in the treatment of chronic visceral pain.
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Chung, S. A., and N. E. Diamant. "Small intestinal motility in fasted and postprandial states: effect of transient vagosympathetic blockade." American Journal of Physiology-Gastrointestinal and Liver Physiology 252, no. 3 (1987): G301—G308. http://dx.doi.org/10.1152/ajpgi.1987.252.3.g301.
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We investigated vagal control of the migrating myoelectric complex (MMC) and postprandial pattern of the canine small intestine. Gastric and small intestinal motility were monitored in six conscious dogs. The vagosympathetic nerves, previously isolated in bilateral skin loops, were blocked by cooling. To feed, a meat-based liquid food was infused by tube into the gastric fundus. MMC phases I, II, III, and IV were observed in the fasted state. On feeding, the fed pattern appeared quickly in the proximal small bowel but was delayed distally. Vagal blockade abolished all gastric contractions and spiking activity as well as the small bowel fed pattern. During vagal blockade, the small bowel exhibited MMC-like migrating bursts of spikes in both the fasted and fed states. The migration and cycling of these bursts were not significantly different from the MMC, but the duodenal and jejunal phase II was absent or shortened. On termination of vagal blockade, normal fasting or fed activity reappeared but with a delay in the fed pattern distally. We conclude: the ileum is the least sensitive to vagal blockade; the fasting vagal influence is exerted primarily on phases I and II of the duodenal and jejunal MMC; the fed pattern throughout the entire small bowel is normally dependent upon vagal integrity; the phase III-like bursts of activity seen during vagal blockade likely represents the intrinsic small bowel MMC, which is vagally independent.
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Dusi, Veronica, and Gaetano Maria De Ferrari. "Vagal stimulation in heart failure." Herz 46, no. 6 (2021): 541–49. http://dx.doi.org/10.1007/s00059-021-05076-5.
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AbstractVagal nerve stimulation (VNS) has a strong pathophysiological rationale as a potentially beneficial treatment for heart failure with reduced ejection fraction. Despite several promising preclinical studies and pilot clinical studies, the two large, controlled trials—NECTAR-HF and INOVATE-HF—failed to demonstrate the expected benefit. It is likely that clinical application of VNS in phase III studies was performed before a sufficient degree of understanding of the complex pathophysiology of autonomic electrical modulation had been achieved, therefore leading to an underestimation of its potential benefit. More knowledge on the complex dose–response issue of VNS (i.e., pulse amplitude, frequency, duration and duty cycle) has been gathered since these trials and a new randomized study is currently underway with an adaptive design and a refined approach in an attempt to deliver the proper dose to a more selected group of patients.
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Ardell, J. L., and W. C. Randall. "Selective vagal innervation of sinoatrial and atrioventricular nodes in canine heart." American Journal of Physiology-Heart and Circulatory Physiology 251, no. 4 (1986): H764—H773. http://dx.doi.org/10.1152/ajpheart.1986.251.4.h764.
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Parasympathetic pathways mediating chronotropic and dromotropic responses to cervical vagal stimulation were determined from sequential, restricted, intrapericardial dissection around major cardiac vessels. Although right cervical vagal input evoked significantly greater bradycardia, supramaximal electrical stimulation of either vagus produced similar ventricular rates, both with and without simultaneous atrial pacing. Dissection of the triangular fat pad at the junction of the inferior vena cava-inferior left atrium (IVC-ILA) invariably eliminated all vagal input to the atrioventricular (AV) nodal region. Yet IVC-ILA dissection had minimal influence on evoked-chronotropic responses to either cervical vagal or stellate ganglia stimulation. Respective intrapericardial projection pathways, from either right or left vagi, are sufficiently distinct to allow unilateral parasympathetic denervation of the sinoatrial (SA) and atrioventricular (AV) nodal regions. Left vagal projections to the SA and AV nodal regions course primarily along and between the right pulmonary artery and left superior pulmonary vein. Right vagal projections to the SA and AV nodal regions are somewhat more diffuse but concentrate around the right pulmonary vein complex and adjacent segments of the right pulmonary artery. We conclude there are parallel, yet functionally distinct, inputs from right and left vagi to the SA and AV nodal regions.
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Tan, Zhenjun, Ronald Fogel, Chunhui Jiang, and Xueguo Zhang. "Galanin Inhibits Gut-Related Vagal Neurons in Rats." Journal of Neurophysiology 91, no. 5 (2004): 2330–43. http://dx.doi.org/10.1152/jn.00869.2003.
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Galanin plays an important role in the regulation of food intake, energy balance, and body weight. Many galanin-positive fibers as well as galanin-positive neurons were seen in the dorsal vagal complex, suggesting that galanin produces its effects by actions involving vagal neurons. In the present experiment, we used tract-tracing and neurophysiological techniques to evaluate the origin of the galaninergic fibers and the effect of galanin on neurons in the dorsal vagal complex. Our results reveal that the nucleus of the solitary tract is the major source of the galanin terminals in the dorsal vagal complex. In vivo experiments demonstrated that galanin inhibited the majority of gut-related neurons in the dorsal motor nucleus of the vagus. In vitro experiments demonstrated that galanin inhibited the majority of stomach-projecting neurons in the dorsal motor nucleus of the vagus by suppressing spontaneous activity and/or producing a fully reversible dose-dependent membrane hyperpolarization and outward current. The galanin-induced hyperpolarization and outward current persisted after synaptic input was blocked, suggesting that galanin acts directly on receptors of neurons in the dorsal motor nucleus of the vagus. The reversal potential induced by galanin was close to the potassium ion potentials of the Nernst equation and was prevented by the potassium channel blocker tetraethylammonium, indicating that the inhibitory effect of galanin was mediated by a potassium channel. These results indicate that the dorsal motor nucleus of the vagus is inhibited by galanin derived predominantly from neurons in the nucleus of the solitary tract projecting to the dorsal motor nucleus of the vagus nerve. Galanin is one of the neurotransmitters involved in the vago-vagal reflex.
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Krowicki, Z. K., A. Arimura, N. A. Nathan, and P. J. Hornby. "Hindbrain effects of PACAP on gastric motor function in the rat." American Journal of Physiology-Gastrointestinal and Liver Physiology 272, no. 5 (1997): G1221—G1229. http://dx.doi.org/10.1152/ajpgi.1997.272.5.g1221.
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Pituitary adenylate cyclase-activating polypeptide (PACAP)-like immunoreactive cell bodies and fibers are visualized in hindbrain nuclei that are involved in the regulation of autonomic function, yet little is known about the gastric and cardiovascular effects of this peptide in the dorsal vagal complex, nucleus raphe obscurus, and nucleus ambiguus. Therefore, multiple-barreled micropipettes were used to inject PACAP-38 (1-100 pmol) into each of these nuclei in alpha-chloralose anesthetized rats, while intragastric pressure, pyloric and greater curvature smooth muscle contractile activity, blood pressure, and heart rate were recorded. For comparison, the effect of L-glutamate (15 nmol) microinjected into the same sites on gastric motor activity was also assessed. L-Glutamate microinjected into each nucleus before PACAP-38 significantly increased intragastric pressure, both in terms of the peak increase and the total area of the response. Microinjections of PACAP-38 (10 and 100 pmol) into each of the nuclei significantly increased peak intragastric pressure, but the total area of the response was only significantly increased by the highest dose (100 pmol) in the case of the dorsal vagal complex and nucleus raphe obscurus. No consistent changes in heart rate and mean arterial blood pressure were noted after microinjection of PACAP-38 into each of the three nuclei. Bilateral vagotomy abolished the increase in intragastric pressure in response to microinjection of PACAP-38 into the dorsal vagal complex and nucleus raphe obscurus. We conclude that PACAP-38 in the dorsal vagal complex and nucleus raphe obscurus is involved in vagally mediated gastric motor excitation.
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Rogers, R. C., D. M. McTigue, and G. E. Hermann. "Vagovagal reflex control of digestion: afferent modulation by neural and "endoneurocrine" factors." American Journal of Physiology-Gastrointestinal and Liver Physiology 268, no. 1 (1995): G1—G10. http://dx.doi.org/10.1152/ajpgi.1995.268.1.g1.
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Vagovagal reflex control circuits in the dorsal vagal complex of the brain stem provide overall coordination of gastric, small intestinal, and pancreatic digestive functions. The neural components forming these reflex circuits are under substantial descending neural control. By adjusting the excitability of the differing components of the reflex, significant alterations in digestion control can be produced by the central nervous system. Additionally, the dorsal vagal complex is situated within a circumventricular region without a "blood-brain barrier." As a result, vagovagal reflex circuitry is also exposed to humoral influences, which can profoundly alter digestive functions by acting directly on brain stem neurons.
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Kollai, M., G. Jokkel, I. Bonyhay, J. Tomcsanyi, and A. Naszlady. "Relation between baroreflex sensitivity and cardiac vagal tone in humans." American Journal of Physiology-Heart and Circulatory Physiology 266, no. 1 (1994): H21—H27. http://dx.doi.org/10.1152/ajpheart.1994.266.1.h21.
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The extent of dependence of cardiac vagal tone on arterial baroreceptor input has been studied in 12 healthy, young adult subjects. Cardiac vagal tone was defined as the chang in R-R interval after complete cholinergic blockade by atropine. Baroreflex sensitivity was determined with the "Oxford-method": R-R interval was regressed against systolic pressure. The interindividual correlation between cardiac vagal tone and baroreflex sensitivity for falling pressures was found to be significant, but not close (R = 0.81, P = 0.002). In each subject, the baroreflex regression line for falling pressures was extrapolated to the post-atropine R-R interval level; 50 mmHg was considered as minimum and 80 mmHg as maximum threshold level for the integrated baroreflex. From the relation between the individual regression lines and the minimum and maximum threshold levels, it was concluded that cardiac vagal tone could be generated by both baroreflex-dependent and -independent mechanisms, the ratio of which varies in different individuals, with the baroreflex-dependent mechanism being the dominant factor.
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Martinmäki, Kaisu, Heikki Rusko, Libbe Kooistra, Joni Kettunen, and Sami Saalasti. "Intraindividual validation of heart rate variability indexes to measure vagal effects on hearts." American Journal of Physiology-Heart and Circulatory Physiology 290, no. 2 (2006): H640—H647. http://dx.doi.org/10.1152/ajpheart.00054.2005.
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Heart rate variability (HRV) has been widely used as a measure of vagal activation in physiological, psychological, and clinical examinations. We studied the within-subject quantitative relationship between HRV and vagal effects on the heart in different body postures during a gradually decreasing vagal blockade. Electrocardiogram and respiratory frequency were measured in subjects (8 endurance athletes and 10 participants of nonendurance sports) in supine, sitting, and standing postures before the blockade, under vagal blockade (atropine sulfate, 0.04 mg/kg), and four times during a 150-min recovery from the blockade. Fast Fourier transform was used to calculate low-frequency power (LFP, 0.04–0.15 Hz), high-frequency power (HFP, 0.15–0.40 Hz), and total power (TP, 0.04–0.40 Hz). A within-subject linear regression analysis of recovery time on each HRV index was conducted. Complete vagal blockade decreased all HRV significantly, particularly HFP ( P < 0.001). A linear fit explained a large portion of the within-subject variance between recovery time and natural log-transformed (ln) HRV indexes in every posture, with coefficients of determination ( R2) in the supine posture [means (SD)]: 98 (SD 2)% for mean R-R interval, 87 (SD 10)% for lnLFP, 87 (SD 13)% for lnHFP, and 91 (SD 10)% for lnTP. Neither body posture nor endurance-training background had an impact on R2 values. There was marked between-subject variation in the R2 values, slopes, and intercepts. In conclusion, all HRV, particularly HFP, is predominantly under vagal control. Within subjects, lnLFP, lnHFP, and lnTP increased linearly with the gradually decreasing vagal blockade in all postures.
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Li, Y., and C. Owyang. "Somatostatin inhibits pancreatic enzyme secretion at a central vagal site." American Journal of Physiology-Gastrointestinal and Liver Physiology 265, no. 2 (1993): G251—G257. http://dx.doi.org/10.1152/ajpgi.1993.265.2.g251.
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The mechanisms and site of action of somatostatin-induced inhibition of pancreatic enzyme secretion were investigated using different stimulants of pancreatic secretion acting on different sites in anesthetized rats. Administration of graded doses of somatostatin-14 resulted in a dose-related inhibition of pancreatic protein secretion evoked by 2-deoxy-D-glucose, a central vagal stimulant that acts by stimulating the dorsal vagal nuclei. The lowest effective dose of somatostatin-14 was 1.0 microgram.kg-1 x h-1; maximal effective dose was 25 micrograms.kg-1 x h-1, which resulted in complete inhibition of protein output. Similarly, somatostatin-14 at a dose of 25 micrograms.kg-1 x h-1 also completely inhibited pancreatic protein secretion in response to a physiological concentration of cholecystokinin octapeptide (CCK-8), which acts via a vagal afferent pathway. In contrast, pancreatic protein outputs evoked by bethanechol, which directly stimulates pancreatic muscarinic receptors, or electrical stimulation of the vagal trunk, which activates the vagal efferent pathway, were unaffected by somatostatin-14. In separate studies, we demonstrated that perivagal treatment with the sensory neurotoxin capsaicin impaired pancreatic responses to CCK-8 but had no effect on the inhibitory action of somatostatin-14 on pancreatic secretion evoked by 2-deoxy-D-glucose, ruling out an effect of somatostatin on the vagal afferent pathway. Similarly we also demonstrated that perineural capsaicin treatment of the celiac-superior mesenteric ganglia did not affect the inhibitory action of somatostatin. These findings indicate that somatostatin inhibits 2-deoxy-D-glucose- and CCK-8-evoked pancreatic enzyme secretion via a vagal pathway.(ABSTRACT TRUNCATED AT 250 WORDS)
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Chung, S. A., G. R. Greenberg, and N. E. Diamant. "Relationship of postprandial motilin, gastrin, and pancreatic polypeptide release to intestinal motility during vagal interruption." Canadian Journal of Physiology and Pharmacology 70, no. 8 (1992): 1148–53. http://dx.doi.org/10.1139/y92-159.
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Experiments were performed to determine how postprandial motilin, gastrin, and pancreatic polypeptide plasma concentrations measured during vagal blockade relate to coincident small intestinal motility patterns. Feeding produced a postprandial pattern of intestinal motility coincident with a sustained increase in gastrin and pancreatic polypeptide and a decline in motilin plasma concentrations. Vagal blockade replaced the fed pattern with one similar to migrating motor complex (MMC) activity. Highest motilin plasma concentrations were observed during phase III of this MMC-like activity, as occurs in the fasted state. Vagal blockade reduced but did not abolish the postprandial increase in plasma gastrin and pancreatic polypeptide concentrations. Termination of vagal cooling produced a decline in motilin and an elevation in gastrin and pancreatic polypeptide concentrations, coincident with the return of the fed pattern. In conclusion, during vagal blockade in the fed state (i) motilin, but not gastrin or pancreatic polypeptide plasma concentrations, fluctuate with the MMC-like activity, and any measurement of motilin concentrations under these circumstances must be interpreted on the basis of gut motility patterns, and (ii) gastrin and pancreatic polypeptide concentrations are marginally elevated, but these changes are not enough to disrupt the MMC or have any motor effect. Lastly, the fed pattern and the postprandial changes in motilin, gastrin, and pancreatic polypeptide concentrations are in part dependent upon intact vagal pathways.Key words: gastrointestinal motility, vagus, motilin, gastrin, pancreatic polypeptide.
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McTigue, D. M., and R. C. Rogers. "Pancreatic polypeptide stimulates gastric acid secretion through a vagal mechanism in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 269, no. 5 (1995): R983—R987. http://dx.doi.org/10.1152/ajpregu.1995.269.5.r983.
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The present study examined the effect of pancreatic polypeptide (PP) on gastric acid secretion. A 45-min infusion of PP was delivered into the jugular vein of urethan-anesthetized rats. Rat PP (100 pmol) significantly increased acid secretion over baseline; bilateral cervical vagotomy or peripheral atropine both eliminated this acid response. Neither intraperitoneal infusion nor close intra-arterial infusion of 100 pmol PP into the gastric circulation altered acid secretion. These results suggest that although PP requires intact vagal reflexes to stimulate acid output, it does not act on afferent or presynaptic efferent terminals of the vagus or directly within the stomach. Given that vagal reflexes consist of an afferent limb, an efferent limb, and a central relay, it may be that the target of circulating PP lies within the central nervous system. Indeed, previous studies from our laboratory have shown that microinjection of PP into the dorsal vagal complex results in long-lasting vagal-dependent elevation of gastric acid secretion.
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Salim, Aws S. "Surgery or chemoneurolysis for complete vagal denervation of rat stomach?" Digestive Diseases and Sciences 36, no. 8 (1991): 1074–78. http://dx.doi.org/10.1007/bf01297449.
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Mazgalev, T., L. S. Dreifus, E. L. Michelson, and A. Pelleg. "Vagally induced hyperpolarization in atrioventricular node." American Journal of Physiology-Heart and Circulatory Physiology 251, no. 3 (1986): H631—H643. http://dx.doi.org/10.1152/ajpheart.1986.251.3.h631.
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The effects of postganglionic vagal stimulation on atrioventricular nodal conduction were studied in 12 rabbit atrial-atrioventricular nodal preparations. Vagal stimulation was introduced in the sinus and atrioventricular nodes, separately or in combination, using single bursts of subthreshold stimuli. The sinus cycle length was scanned to identify the phasic effect of vagal stimulation. Action potentials from cells in the AN, N, and NH regions of the atrioventricular node were recorded by microelectrode techniques. Vagally induced hyperpolarization of cells in the atrioventricular node resulted in a phase-dependent prolongation of conduction time and reflected the level of residual hyperpolarization at the moment of arrival of the next atrial beat at the atrioventricular nodal input region. Vagally induced hyperpolarization was membrane potential dependent, although its overall time course was similar at different phases. Increased diastolic depolarization followed the maximal hyperpolarization. This "rebound" observed at certain phases was responsible for paradoxical shortening of the conduction time after vagal stimulation. The predominant effects of local vagal stimulation in the atrioventricular node were observed in cells in or near the N region. Slower rate of rise, shorter amplitude and duration, as well as step formations were among the changes in action potentials recorded from these cells. The effects of vagal stimulation were inhomogeneous between different regions of the atrioventricular node as well as within the N region, producing alternative pathways of conduction and the potential for reentry. The concomitant changes in sinus cycle length resulting from vagal stimulation in the sinus node region altered the phasic effects of vagal stimulation introduced in the atrioventricular node. This was related to a direct influence of the prolonged sinus cycle length on atrioventricular nodal refractoriness as well as an indirect effect on the degree of residual vagally induced hyperpolarization at the moment of arrival of the delayed atrial beat. These findings provide mechanistic explanations for the complex effects of vagal stimulation on atrioventricular nodal conduction.
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Fernandes, Camila. "Figuras do constrangimento: As instituições de Estado e as políticas de acusação sexual." Mana 25, no. 2 (2019): 365–90. http://dx.doi.org/10.1590/1678-49442019v25n2p365.
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Resumo O artigo explora como se arquiteta um discurso de acusação em torno da sexualidade feminina “irresponsável” no interior de instituições públicas. A discussão parte de etnografia realizada em creches públicas situadas num complexo de favelas da Zona Norte (RJ). Apresento as principais etapas de acesso às vagas na instituição, assim como as estratégias mobilizadas pelas famílias para conseguir uma vaga. Acompanho de que maneira algumas situações são conduzidas a partir de uma pedagogia do constrangimento, nas quais “esporros” públicos configuram um campo de tensão entre funcionárias e mulheres usuárias dos serviços. A relação entre mulheres é marcada pela ambivalência de uma ação administrativa que, ao mesmo tempo em que acolhe as demandas pelo cuidado das crianças, é feita de censuras e constrangimentos morais. Ao final, discuto a presença de um Estado feminino, uma ação que mescla qualidades de cuidado ao lado de expedientes de cobrança e responsabilização.
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Emch, Gregory S., Gerlinda E. Hermann та Richard C. Rogers. "TNF-α activates solitary nucleus neurons responsive to gastric distension". American Journal of Physiology-Gastrointestinal and Liver Physiology 279, № 3 (2000): G582—G586. http://dx.doi.org/10.1152/ajpgi.2000.279.3.g582.
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Tumor necrosis factor-α (TNF-α) is liberated as part of the immune response to antigenic challenge, carcinogenesis, and radiation therapy. Previous studies have implicated elevated circulating levels of this cytokine in the gastric hypomotility associated with these disease states. Our earlier studies suggest that a site of action of TNF-α may be within the medullary dorsal vagal complex. In this study, we describe the role of TNF-α as a neuromodulator affecting neurons in the nucleus of the solitary tract that are involved in vago-vagal reflex control of gastric motility. The results presented herein suggest that TNF-α may induce a persistent gastric stasis by functioning as a hormone that modulates intrinsic vago-vagal reflex pathways during illness.
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Gujrathi, Atishkumar B., Vijayalaxmi Ambulgekar, and Shrinivas Chavan. "Vagal Nerve Schwannoma: Presentation of Two Case Reports." An International Journal of Otorhinolaryngology Clinics 8, no. 3 (2016): 116–18. http://dx.doi.org/10.5005/jp-journals-10003-1246.
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ABSTRACT Vagal nerve schwannomas are rare neural sheath tumors. Although schwannomas are generally benign lesions, they are known to enlarge at a rate of 2.5 to 3 mm per year according to published reports. Vagal nerve schwannoma usually occurs between the 3rd and 5th decades of life, it does not show sex predilection, with both sexes being equally affected, and it most often presents as a painless, slow-growing, lateral neck mass. The treatment of choice is complete surgical excision with preservation of the neural pathway, when it is possible. These tumors, in fact, are almost always benign, and a conservative surgical approach is emphasized by most of the authors. Here, we are presenting two cases of cervical vagal schwannoma, both were middle aged females and presenting in the ear, nose, and throat (ENT) department as a painless lateral neck swelling and were operated by horizontal skin crease incision. Of the two cases, we succeeded to secure nerve functions in one case. The clinical features, diagnosis, management, and pathological findings of cervical vagal schwannoma are discussed. How to cite this article Gujrathi AB, Ambulgekar V, Chavan S. Vagal Nerve Schwannoma: Presentation of Two Case Reports. Int J Otorhinolaryngol Clin 2016;8(3):116-118.
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van de Wall, E. H. E. M., P. Duffy, and R. C. Ritter. "CCK enhances response to gastric distension by acting on capsaicin-insensitive vagal afferents." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 289, no. 3 (2005): R695—R703. http://dx.doi.org/10.1152/ajpregu.00809.2004.
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Capsaicin treatment destroys vagal afferent C fibers and markedly attenuates reduction of food intake and induction of hindbrain Fos expression by CCK. However, both anatomical and electrophysiological data indicate that some gastric vagal afferents are not destroyed by capsaicin. Because CCK enhances behavioral and electrophysiological responses to gastric distension in rats and people, we hypothesized that CCK might enhance the vagal afferent response to gastric distension via an action on capsaicin-insensitive vagal afferents. To test this hypothesis, we quantified expression of Fos-like immunoreactivity (Fos) in the dorsal vagal complex (DVC) of capsaicin-treated (Cap) and control rats (Veh), following gastric balloon distension alone and in combination with CCK injection. In Veh rats, intraperitoneal CCK significantly increased DVC Fos, especially in nucleus of the solitary tract (NTS), whereas in Cap rats, CCK did not significantly increase DVC Fos. In contrast to CCK, gastric distension did significantly increase Fos expression in the NTS of both Veh and Cap rats, although distension-induced Fos was attenuated in Cap rats. When CCK was administered during gastric distension, it significantly enhanced NTS Fos expression in response to distension in Cap rats. Furthermore, CCK's enhancement of distension-induced Fos in Cap rats was reversed by the selective CCK-A receptor antagonist lorglumide. We conclude that CCK directly activates capsaicin-sensitive C-type vagal afferents. However, in capsaicin-resistant A-type afferents, CCK's principal action may be facilitation of responses to gastric distension.
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Lee, Kun-Ze, Milapjit S. Sandhu, Brendan J. Dougherty, Paul J. Reier, and David D. Fuller. "Influence of vagal afferents on supraspinal and spinal respiratory activity following cervical spinal cord injury in rats." Journal of Applied Physiology 109, no. 2 (2010): 377–87. http://dx.doi.org/10.1152/japplphysiol.01429.2009.
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C2 spinal hemisection (C2HS) interrupts ipsilateral bulbospinal pathways and induces compensatory increases in contralateral spinal and possibly supraspinal respiratory output. Our first purpose was to test the hypothesis that after C2HS contralateral respiratory motor outputs become resistant to vagal inhibitory inputs associated with lung inflation. Bilateral phrenic and contralateral hypoglossal (XII) neurograms were recorded in anesthetized and ventilated rats. In uninjured (control) rats, lung inflation induced by positive end-expired pressure (PEEP; 3–9 cmH2O) robustly inhibited both phrenic and XII bursting. At 2 wk post-C2HS, PEEP evoked a complex response associated with phrenic bursts of both reduced and augmented amplitude, but with no overall change in the mean burst amplitude. PEEP-induced inhibition of XII bursting was still present but was attenuated relative to controls. However, by 8 wk post-C2HS PEEP-induced inhibition of both phrenic and XII output were similar to that in controls. Our second purpose was to test the hypothesis that vagal afferents inhibit ipsilateral phrenic bursting, thereby limiting the incidence of the spontaneous crossed phrenic phenomenon in vagal-intact rats. Bilateral vagotomy greatly enhanced ipsilateral phrenic bursting, which was either weak or absent in vagal-intact rats at both 2 and 8 wk post-C2HS. We conclude that 1) compensatory increases in contralateral phrenic and XII output after C2HS blunt the inhibitory influence of vagal afferents during lung inflation and 2) vagal afferents robustly inhibit ipsilateral phrenic bursting. These vagotomy data appear to explain the variability in the literature regarding the onset of the spontaneous crossed phrenic phenomenon in spontaneously breathing (vagal intact) vs. ventilated (vagotomized) preparations.
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Porta, A., P. Castiglioni, M. Di Rienzo, et al. "Short-term complexity indexes of heart period and systolic arterial pressure variabilities provide complementary information." Journal of Applied Physiology 113, no. 12 (2012): 1810–20. http://dx.doi.org/10.1152/japplphysiol.00755.2012.
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It is unclear whether the complexity of the variability of the systolic arterial pressure (SAP) provides complementary information to that of the heart period (HP). The complexity of HP and SAP variabilities was assessed from short beat-to-beat recordings (i.e., 256 cardiac beats). The evaluation was made during a pharmacological protocol that induced vagal blockade with atropine or a sympathetic blockade (beta-adrenergic blockade with propranolol or central sympathetic blockade with clonidine) alone or in combination, during a graded head-up tilt, and in patients with Parkinson's disease (PD) without orthostatic hypotension undergoing orthostatic challenge. Complexity was quantified according to the mean square prediction error (MSPE) derived from univariate autoregressive (AR) and multivariate AR (MAR) models. We found that: 1) MSPEMAR did not provide additional information to that of MSPEAR; 2) SAP variability was less complex than that of HP; 3) because HP complexity was reduced by either vagal blockade or vagal withdrawal induced by head-up tilt and was unaffected by beta-adrenergic blockade, HP was under vagal control; 4) because SAP complexity was increased by central sympathetic blockade and was unmodified by either vagal blockade or vagal withdrawal induced by head-up tilt, SAP was under sympathetic control; 5) SAP complexity was increased in patients with PD; and 6) during orthostatic challenge, the complexity of both HP and SAP variabilities in patients with PD remained high, thus indicating both vagal and sympathetic impairments. Complexity indexes derived from short HP and SAP beat-to-beat series provide complementary information and are helpful in detecting early autonomic dysfunction in patients with PD well before circulatory symptoms become noticeable.
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Satpathy, Shouvanik, Goutam Mondal, Anup Kumar Bhowmick, and Aniruddha Dam. "Cervical Vagal Swannoma: A Case Report." Bangladesh Journal of Otorhinolaryngology 21, no. 2 (2016): 115–18. http://dx.doi.org/10.3329/bjo.v21i2.27651.
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Cervical vagal schwannomas are rare, slow growing tumours usually occur in patients between thirty and fifty years of age with no sex related predisposition. They are usually asymptomatic benign lesion and complete surgical resection with preservation of neural pathway, whenever possible is the treatment of choice.Bangladesh J Otorhinolaryngol; October 2015; 21(2): 115-118
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Ekmekçi, Hakan, and Hülagu Kaptan. "Vagal Nerve Stimulation." Open Access Macedonian Journal of Medical Sciences 5, no. 3 (2017): 391–94. http://dx.doi.org/10.3889/oamjms.2017.056.
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BACKGROUND: The vagus nerve stimulation (vns) is an approach mainly used in cases of intractable epilepsy despite all the efforts. Also, its benefits have been shown in severe cases of depression resistant to typical treatment.AIM: The aim of this study was to present current knowledge of vagus nerve stimulation.MATERIAL AND METHODS: A new value has emerged just at this stage: VNS aiming the ideal treatment with new hopes. It is based on the placement of a programmable generator on the chest wall. Electric signals from the generator are transmitted to the left vagus nerve through the connection cable. Control on the cerebral bioelectrical activity can be achieved by way of these signal sent from there in an effort for controlling the epileptic discharges.RESULTS: The rate of satisfactory and permanent treatment in epilepsy with monotherapy is around 50%. This rate will increase by one-quarters (25%) with polytherapy. However, there is a patient group roughly constituting one-thirds of this population, and this group remains unresponsive or refractory to all the therapies and combined regimes. The more the number of drugs used, the more chaos and side effects are observed. The anti-epileptic drugs (AEDs) used will have side effects on both the brain and the systemic organs. Cerebral resection surgery can be required in some patients. The most commonly encountered epilepsy type is the partial one, and the possibility of benefiting from invasive procedures is limited in most patients of this type. Selective amygdala-hippocampus surgery is a rising value in complex partial seizures. Therefore, as epilepsy surgery can be performed in very limited numbers and rather developed centres, success can also be achieved in limited numbers of patients. The common ground for all the surgical procedures is the target of preservation of memory, learning, speaking, temper and executive functions as well as obtaining a good control on seizures. However, the action mechanism of VNS is still not exactly known. On the other hand, it appears to be a reliable method that is tolerated well in partial resistant seizures. It has been observed that adverse effects are generally of mild-medium severity, and most of the problems can be eliminated easily through the re-adjustment of the stimulator.CONCLUSION: VNS, which is a treatment modality that will take place it deserves in epilepsy treatment with "the correct patient" and "correct reason", must be known better and its applications must be developed.
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Travagli, R. Alberto, and Richard C. Rogers. "V. Fast and slow extrinsic modulation of dorsal vagal complex circuits." American Journal of Physiology-Gastrointestinal and Liver Physiology 281, no. 3 (2001): G595—G601. http://dx.doi.org/10.1152/ajpgi.2001.281.3.g595.
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Vago-vagal reflex circuits in the medulla are responsible for the smooth coordination of the digestive processes carried out from the oral cavity to the transverse colon. In this themes article, we concentrate mostly on electrophysiological studies concerning the extrinsic modulation of these vago-vagal reflex circuits, with a particular emphasis on two types of modulation, i.e., by “fast” classic neurotransmitters and by “slow” neuromodulators. These examples review two of the most potent modulatory processes at work within the dorsal vagal complex, which have dramatic effects on gastrointestinal function. The reader should be mindful of the fact that many more different inputs from other central nervous system (CNS) loci or circulating humoral factors add to this complex mix of modulatory inputs. It is likely that similar long-term modulations of synaptic transmission occur with other neurotransmitters and may represent an important mechanism for the integration and regulation of neuronal behavior. Of course, this fact strongly militates against the success of any single drug or approach in the treatment of motility disorders having a CNS component.
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Latiș, Sandra-Maria-Vanessa, Alexandru-Dan Costache, Cristina Adam, Magda-Valeria Mitu, and Florin Mitu. "Vagal Maneuvers in Treating Acute Supraventricular Tachycardia with Narrow QRS." Internal Medicine 20, no. 3 (2023): 37–42. http://dx.doi.org/10.2478/inmed-2023-0257.
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Abstract Treatment of supraventricular tachycardia with narrow QRS complexes (SVT) includes different therapeutic strategies such as: cardioversion, drug therapy or vagal maneuvers, depending on the patient’s condition, especially if they are hemodynamically stable or unstable. Vagal maneuvers are used to treat SVT during the acute presentation, if the patient is stable. They are recommended by the 2019 European Society of Cardiology guidelines for management of SVT with narrow QRS complexes. These include the Valsalva maneuver (enhanced or not) and carotid sinus massage. They have multiple advantages: they do not require medical equipment, can be performed anywhere (at the bedside or in an outpatient setting), have minimal risk and high effectiveness (19-54 % rate of success).
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Yost, Bethany L., Gerald J. Gleich, David B. Jacoby, and Allison D. Fryer. "The changing role of eosinophils in long-term hyperreactivity following a single ozone exposure." American Journal of Physiology-Lung Cellular and Molecular Physiology 289, no. 4 (2005): L627—L635. http://dx.doi.org/10.1152/ajplung.00377.2004.
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Ozone hyperreactivity over 24 h is mediated by blockade of inhibitory M2 muscarinic autoreceptors by eosinophil major basic protein. Because eosinophil populations in the lungs fluctuate following ozone, the contribution of eosinophils to M2 dysfunction and airway hyperreactivity was measured over several days. After one exposure to ozone, M2 function, vagal reactivity, smooth muscle responsiveness, and inflammation were measured in anesthetized guinea pigs. Ozone-induced hyperreactivity to vagal stimulation persisted over 3 days. Although hyperreactivity one day after ozone is mediated by eosinophils, AbVLA-4 did not inhibit either eosinophil accumulation in the lungs or around the nerves or prevent hyperreactivity at this time point. Two days after ozone, eosinophils in BAL, around airway nerves and in lungs, were decreased, and neuronal M2 receptor function was normal, although animals were still hyperreactive to vagal stimulation. Depleting eosinophils with AbIL-5 prevented hyperreactivity, thus eosinophils contribute to vagal hyperreactivity by mechanisms separate from M2 receptor blockade. Three days after ozone, vagal hyperreactivity persisted, eosinophils were again elevated in BAL in lungs and around nerves, and M2 receptors were again dysfunctional. At this point, airway smooth muscle was also hyperresponsive to methacholine. Eosinophil depletion with AbIL-5, AbVLA-4, or cyclophosphamide protected M2 function 3 days after ozone and prevented smooth muscle hyperreactivity. However, vagal hyperreactivity was significantly potentiated by eosinophil depletion. The site of hyperreactivity, muscle or nerve, changes over 3 days after a single exposure to ozone. Additionally, the role of eosinophils is complex; they mediate hyperreactivity acutely while chronically may be involved in repair.
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Hall, K. E., T. Y. el-Sharkawy, and N. E. Diamant. "Vagal control of canine postprandial upper gastrointestinal motility." American Journal of Physiology-Gastrointestinal and Liver Physiology 250, no. 4 (1986): G501—G510. http://dx.doi.org/10.1152/ajpgi.1986.250.4.g501.
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The role of the vagus nerves in the control of postprandial motility in the upper gastrointestinal tract was investigated in four dogs by use of a bilateral cervical cooling blockade technique. On administration of food, the fasting migrating motor complex (MMC) was replaced by the postprandial (feeding) pattern. Feeding pattern duration varied in a dose-dependent manner with either total volume or calories of food. During the feeding pattern, oscillations in lower esophageal sphincter (LES) pressure occurred at time intervals equivalent to the MMC cycle period. Twenty-one control feeding experiments and 17 postprandial vagal blockade experiments were performed, with a minimum of three of each type in each dog. Vagal blockade, initiated at times ranging from 15 min to 4 h after feeding and maintained for up to 5 h, abolished the postprandial activity in the upper gastrointestinal tract. During postprandial vagal blockade, LES pressure was abolished and bursts of contractions were observed only in the upper small bowel, a pattern resembling that observed during vagal blockade in the fasted state. These bursts occurred at the expected times relative to, and their cycle period was not significantly different from, that of the MMCs recorded prior to feeding. Vagal blockade started prior to feeding prevented initiation of the fed pattern, which appeared immediately on termination of the blockade. We conclude that initiation and maintenance of the postprandial pattern in the upper gastrointestinal tract with concurrent inhibition of the fasting MMC normally require vagal integrity. The "clock" controlling the MMC cycle period is not reset by feeding, but its effect on motility is suppressed.
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Jammes, Y. "Tonic sensory pathways of the respiratory system." European Respiratory Journal 1, no. 2 (1988): 176–83. http://dx.doi.org/10.1183/09031936.93.01020176.
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Both respiratory centres and the preganglionic vagal motoneurones, which control respiratory (striated) and airway (smooth) muscles respectively, receive information on the lungs, the circulation and the skeletal and respiratory muscles. Each of these nervous pathways has two components: one is phasic, i.e. in phase with biological rhythms, and comes from mechanoreceptors connected to large myelinated fibres; the second has a tonic low frequency firing rate and corresponds to the spontaneous activity of polymodal receptors connected to thin sensory fibres, which act mostly as sensors of changes in extracellular fluid composition (O2 and/or CO2 partial pressure, pH, release of algesic agents etc...). Some of them also detect large mechanical disturbances or local temperature changes. The influence of tonic background sensory activity is well known in animals concerning the role played by arterial chemoreceptors in the control of ventilation and of thin vagal afferents from the lungs (bronchopulmonary C-fibres and irritant receptors) in reflex facilitation of the bronchoconstrictor vagal tone. Moreover, the stimulation of thin sensory fibres in particular circumstances is responsible for hyperventilation (arterial chemoreceptors and muscle afferents), increased airway tone (arterial chemoreceptors and mostly thin vagal afferent fibres) or bronchodilation (muscle afferents). These peripheral inputs project centrally on different structures and also on brain stem neurones, which integrate simultaneously chemosensory, vagal and muscle information. This results in complex interactions between the different sensory pathways.
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Armour, J. A., and W. C. Randall. "Rebound cardiovascular responses following stimulation of canine vagosympathetic complexes or cardiopulmonary nerves." Canadian Journal of Physiology and Pharmacology 63, no. 9 (1985): 1122–32. http://dx.doi.org/10.1139/y85-184.
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Electrical stimulation of a canine vagosympathetic complex or a cardiopulmonary nerve can elicit a variety of negative chronotropic and inotropic cardiac responses, with or without alterations in systemic arterial pressure. In the period immediately following cessation of such a stimulation "rebound" tachycardia, increased inotropism above control values in one or more regions of the heart, and (or) elevation in systemic arterial pressure can occur. These "rebound" phenomena are abolished by propranolol or ipsilateral chronic sympathectomy. It is proposed that "vagal" poststimulation "rebound" of the canine cardiovascular system is primarily the result of activation of sympathetic neural elements present in the vagosympathetic complexes or cardiopulmonary nerves.
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Poli, Andrea, Angelo Gemignani, Federico Soldani, and Mario Miccoli. "A Systematic Review of a Polyvagal Perspective on Embodied Contemplative Practices as Promoters of Cardiorespiratory Coupling and Traumatic Stress Recovery for PTSD and OCD: Research Methodologies and State of the Art." International Journal of Environmental Research and Public Health 18, no. 22 (2021): 11778. http://dx.doi.org/10.3390/ijerph182211778.
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Baseline respiratory sinus arrhythmia (RSA) has been proposed as a transdiagnostic biomarker of stress vulnerability across psychopathologies, and a reliable association between PTSD, OCD and lower resting RSA was found. Contemplative practices have been linked to the activation of the vagus as well as to an increased RSA that, according to the polyvagal theory, reflects the activation of the ventral vagal complex (VVC) and may promote PTSD and OCD recovery. PubMed and Scopus databases were selected to conduct a search following the Preferred Reporting Items for Systematic Review and Meta-Analyses (PRISMA) 2020 guidelines, and A MeaSurement Tool to Assess systematic Reviews-2 (AMSTAR-2) was used to appraise the methodological quality for this systematic review. Six articles met the inclusion criteria (one cross-sectional study, one study with pre-post measurements, two cohort studies and two RCT studies). Mindfulness-related interventions promoted parasympathetic activity, an increased vagal tone and improvements in PTSD and OCD symptoms. According to the polyvagal theory, mindfulness-related and compassion-related meditations would be conceptualized as neural exercises expanding the capacity of the ventral vagal complex to regulate the present state and to promote resilience. Clinical and methodological issues are discussed.
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Adriaensen, Dirk, Inge Brouns, Isabel Pintelon, Ian De Proost, and Jean-Pierre Timmermans. "Evidence for a role of neuroepithelial bodies as complex airway sensors: comparison with smooth muscle-associated airway receptors." Journal of Applied Physiology 101, no. 3 (2006): 960–70. http://dx.doi.org/10.1152/japplphysiol.00267.2006.
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The epithelium of intrapulmonary airways in many species harbors diffusely spread innervated groups of neuroendocrine cells, called neuroepithelial bodies (NEBs). Data on the location, morphology, and chemical coding of NEBs in mammalian lungs are abundant, but none of the proposed functions has so far been fully established. Besides C-fiber afferents, slowly adapting stretch receptors, and rapidly adapting stretch receptors, recent reviews have added NEBs to the list of presumed sensory receptors in intrapulmonary airways. Physiologically, the innervation of NEBs, however, remains enigmatic. This short overview summarizes our present understanding of the chemical coding and exact location of the receptor end organs of myelinated vagal airway afferents in intrapulmonary airways. The profuse populations that selectively contact complex pulmonary NEB receptors are compared with the much smaller group of smooth muscle-associated airway receptors. The main objective of our contribution was to stimulate the idea that the different populations of myelinated vagal afferents that selectively innervate intraepithelial pulmonary NEBs may represent subpopulations of the extensive group of known electrophysiologically characterized myelinated vagal airway receptors. Future efforts should be directed toward finding out which airway receptor groups are selectively coupled to the complex NEB receptors.
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Bendeck, M. P., and R. P. E. Reynolds. "Gastric and duodenal motility in the cat: the role of central innervation assessed by transient vagal blockade." Canadian Journal of Physiology and Pharmacology 64, no. 6 (1986): 712–16. http://dx.doi.org/10.1139/y86-119.
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Experiments were performed on four cats to characterize fasting gastric and small bowel motility and to assess the role of extrinsic vagal innervation in the control of that motor activity. A multilumen manometry tube was positioned to record pressure changes from the proximal small bowel and stomach. Transient vagal nerve blockade was accomplished by cooling the cervical vagosympathetic nerve trunks, previously isolated in skin loops on each side of the neck. Two characteristic patterns of basal activity were documented in the stomach: (i) regular phasic contractions of variable amplitude in the body of the stomach; and (ii) infrequent, irregular contractions of high amplitude in the distal antrum. In the duodenum, two predominant activity patterns were noted: (i) periods of continuous irregular activity; and (ii) irregular clusters of contractions separated by quiescent intervals. No typical migrating motor complex activity was seen in the basal gastric or small bowel recordings. Bilateral vagal blockade did not consistently change the general pattern of gastric or small bowel activity, but did appear to reduce gastric contractile activity, as measured by motility indices. We conclude that extrinsic vagal innervation does not play a major role in the control of fasting feline gastric and duodenal motility.
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Hermann, G. E., G. S. Emch, C. A. Tovar, and R. C. Rogers. "c-Fos generation in the dorsal vagal complex after systemic endotoxin is not dependent on the vagus nerve." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 280, no. 1 (2001): R289—R299. http://dx.doi.org/10.1152/ajpregu.2001.280.1.r289.
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The present study used activation of the c-Fos oncogene protein within neurons in the dorsal vagal complex (DVC) as a marker of neuronal excitation in response to systemic endotoxin challenge [i.e., lipopolysaccharide (LPS)]. Specifically, we investigated whether vagal connections with the brain stem are necessary for LPS cytokine- induced activation of DVC neurons. Systemic exposure to LPS elicited a significant activation of c-Fos in neurons in the nucleus of the solitary tract (NST) and area postrema of all thiobutabarbital-anesthetized rats examined, regardless of the integrity of their vagal nerves. That is, rats with both vagi cervically transected were still able to respond with c-Fos activation of neurons in the DVC. Unilateral cervical vagotomy produced a consistent but small reduction in c-Fos activation in the ipsilateral NST of all animals within this experimental group. Given that afferent input to the NST is exclusively excitatory, it is not surprising that unilateral elimination of all vagal afferents would diminish NST responsiveness (on the vagotomized side). These data lead us to conclude that the NST itself is a primary central nervous system detector of cytokines.
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Higa, Keila T., Eliana Mori, Fabiano F. Viana, Mariana Morris, and Lisete C. Michelini. "Baroreflex control of heart rate by oxytocin in the solitary-vagal complex." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 282, no. 2 (2002): R537—R545. http://dx.doi.org/10.1152/ajpregu.00806.2000.
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Previous work demonstrated that oxytocinergic projections to the solitary vagal complex are involved in the restraint of exercise-induced tachycardia (2). In the present study, we tested the idea that oxytocin (OT) terminals in the solitary vagal complex [nucleus of the solitary tract (NTS)/dorsal motor nucleus of the vagus (DMV)] are involved in baroreceptor reflex control of heart rate (HR). Studies were conducted in male rats instrumented for chronic cardiovascular monitoring with a cannula in the NTS/DMV for brain injections. Basal mean arterial pressure and HR and reflex HR responses during loading and unloading of the baroreceptors (phenylephrine/sodium nitroprusside intravenously) were recorded after administration of a selective OT antagonist (OTant) or OT into the NTS/DMV. The NTS/DMV was selected for study because this region contains such a specific and dense concentration of OT-immunoreactive terminals. Vehicle injections served as a control. OT and OTant changed baroreflex control of HR in opposite directions. OT (20 pmol) increased the maximal bradycardic response (from −56 ± 9 to −75 ± 11 beats/min), whereas receptor blockade decreased the bradycardia (from −61 ± 13 to −35 ± 2 beats/min). OTant also reduced the operating range of the reflex, thus decreasing baroreflex gain (from −5.68 ± 1.62 to −2.83 ± 1.05 beats · min−1 · mmHg−1). OT injected into the NTS/DMV of atenolol-treated rats still potentiated the bradycardic responses to pressor challenges, whereas OT injections had no effect in atropine-treated rats. The brain stem effect was specific because neither vehicle administration nor injection of OT or OTant into the fourth cerebral ventricle had any effect. Our data suggest that OT terminals in the solitary vagal complex modulate reflex control of the heart, acting to facilitate vagal outflow and the slowdown of the heart.
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Facchini, Mario, Gaetano M. De Ferrari, Oscar Bonazzi, Theodore Weiss, and Peter J. Schwartz. "Effect of reflex vagal activation on frequency of ventricular premature complexes." American Journal of Cardiology 68, no. 4 (1991): 349–54. http://dx.doi.org/10.1016/0002-9149(91)90830-e.
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Demir, Semahat S., John W. Clark, and Wayne R. Giles. "Parasympathetic modulation of sinoatrial node pacemaker activity in rabbit heart: a unifying model." American Journal of Physiology-Heart and Circulatory Physiology 276, no. 6 (1999): H2221—H2244. http://dx.doi.org/10.1152/ajpheart.1999.276.6.h2221.
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We have extended our compartmental model [ Am. J. Physiol. 266 ( Cell Physiol. 35): C832–C852, 1994] of the single rabbit sinoatrial node (SAN) cell so that it can simulate cellular responses to bath applications of ACh and isoprenaline as well as the effects of neuronally released ACh. The model employs three different types of muscarinic receptors to explain the variety of responses observed in mammalian cardiac pacemaking cells subjected to vagal stimulation. The response of greatest interest is the ACh-sensitive change in cycle length that is not accompanied by a change in action potential duration or repolarization or hyperpolarization of the maximum diastolic potential. In this case, an ACh-sensitive K+ current is not involved. Membrane hyperpolarization occurs in response to much higher levels of vagal stimulation, and this response is also mimicked by the model. Here, an ACh-sensitive K+ current is involved. The well-known phase-resetting response of the SAN cell to single and periodically applied vagal bursts of impulses is also simulated in the presence and absence of the β-agonist isoprenaline. Finally, the responses of the SAN cell to longer continuous trains of periodic vagal stimulation are simulated, and this can result in the complete cessation of pacemaking. Therefore, this model is 1) applicable over the full range of intensity and pattern of vagal input and 2) can offer biophysically based explanations for many of the phenomena associated with the autonomic control of cardiac pacemaking.
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GÖKSEL, ONUR SELÇUK, Emre Gok, Celalettin Karatepe, et al. "Vascular Tumors of the Neck in Adults: 10-Year Experience in a Tertiary Center." Heart Surgery Forum 23, no. 4 (2020): E493—E497. http://dx.doi.org/10.1532/hsf.2769.
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Introduction: The diagnosis and management of vascular lesions of the neck is a challenging task that requires a multidisciplinary approach. This retrospective study assesses the single center experience of vascular tumors of the neck. Materials and methods: Patients diagnosed with a vascular tumor and/or a mass in close proximity to the carotid artery were identified from our records over a 10-year period. The demographic characteristics, clinical features, surgical approach, and outcomes were reviewed. Results: Surgical excision of 17 vascular lesions were performed in 16 patients with a mean age of 51.56 ± 17.35 years at the time of operation. Intra- and/or postoperative clinical and histological assessment revealed unilateral glomus caroticum (N = 11), glomus vagale (N = 2), bilateral glomus caroticum (N = 1), cavernous hemangioma (N = 1), and carotid sheath tumor (N = 1). In three patients, internal carotid artery, common carotid artery and vagal nerve were sacrificed to facilitate complete tumor excision. During the follow-up period, no tumor recurrences were observed, and the morbidity and mortality were minimal. Conclusion: Preoperative evaluation concerning the size, extent, and anatomical relationships of the tumor thoroughly should be investigated. Multidisciplinary approach involving vascular surgery, otolaryngology, and radiology is preferred to treat these patients for better outcomes. Preoperative embolization in selected cases may decrease estimated blood loss and operative time.
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Babic, Tanja, Ruchi Bhagat, Shuxia Wan, et al. "Role of the vagus in the reduced pancreatic exocrine function in copper-deficient rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 304, no. 4 (2013): G437—G448. http://dx.doi.org/10.1152/ajpgi.00402.2012.
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Copper plays an essential role in the function and development of the central nervous system and exocrine pancreas. Dietary copper limitation is known to result in noninflammatory atrophy of pancreatic acinar tissue. Our recent studies have suggested that vagal motoneurons regulate pancreatic exocrine secretion (PES) by activating selective subpopulations of neurons within vagovagal reflexive neurocircuits. We used a combination of in vivo, in vitro, and immunohistochemistry techniques in a rat model of copper deficiency to investigate the effects of a copper-deficient diet on the neural pathways controlling PES. Duodenal infusions of Ensure or casein, as well as microinjections of sulfated CCK-8, into the dorsal vagal complex resulted in an attenuated stimulation of PES in copper-deficient animals compared with controls. Immunohistochemistry of brain stem slices revealed that copper deficiency reduced the number of tyrosine hydroxylase-immunoreactive, but not neuronal nitric oxide synthase- or choline acetyltransferase-immunoreactive, neurons in the dorsal motor nucleus of the vagus (DMV). Moreover, a copper-deficient diet reduced the number of large (>11 neurons), but not small, intrapancreatic ganglia. Electrophysiological recordings showed that DMV neurons from copper-deficient rats are less responsive to CCK-8 or pancreatic polypeptide than are DMV neurons from control rats. Our results demonstrate that copper deficiency decreases efferent vagal outflow to the exocrine pancreas. These data indicate that the combined selective loss of acinar pancreatic tissue and the decreased excitability of efferent vagal neurons induce a deficit in the vagal modulation of PES.
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Campos, Carlos A., Jason S. Wright, Krzysztof Czaja, and Robert C. Ritter. "CCK-Induced Reduction of Food Intake and Hindbrain MAPK Signaling Are Mediated by NMDA Receptor Activation." Endocrinology 153, no. 6 (2012): 2633–46. http://dx.doi.org/10.1210/en.2012-1025.
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The dorsal vagal complex of the hindbrain, including the nucleus of the solitary tract (NTS), receives neural and humoral afferents that contribute to the process of satiation. The gut peptide, cholecystokinin (CCK), promotes satiation by activating gastrointestinal vagal afferents that synapse in the NTS. Previously, we demonstrated that hindbrain administration of N-methyl-d-aspartate (NMDA)-type glutamate receptor antagonists attenuate reduction of food intake after ip CCK-8 injection, indicating that these receptors play a necessary role in control of food intake by CCK. However, the signaling pathways through which hindbrain NMDA receptors contribute to CCK-induced reduction of food intake have not been investigated. Here we report CCK increases phospho-ERK1/2 in NTS neurons and in identified vagal afferent endings in the NTS. CCK-evoked phospho-ERK1/2 in the NTS was attenuated in rats pretreated with capsaicin and was abolished by systemic injection of a CCK1 receptor antagonist, indicating that phosphorylation of ERK1/2 occurs in and is mediated by gastrointestinal vagal afferents. Fourth ventricle injection of a competitive NMDA receptor antagonist, prevented CCK-induced phosphorylation of ERK1/2 in hindbrain neurons and in vagal afferent endings, as did direct inhibition of MAPK kinase. Finally, fourth ventricle administration of either a MAPK kinase inhibitor or NMDA receptor antagonist prevented the reduction of food intake by CCK. We conclude that activation of NMDA receptors in the hindbrain is necessary for CCK-induced ERK1/2 phosphorylation in the NTS and consequent reduction of food intake.
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Hayes, Matthew R., Scott E. Kanoski, Bart C. De Jonghe, et al. "The common hepatic branch of the vagus is not required to mediate the glycemic and food intake suppressive effects of glucagon-like-peptide-1." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 301, no. 5 (2011): R1479—R1485. http://dx.doi.org/10.1152/ajpregu.00356.2011.
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The incretin and food intake suppressive effects of intraperitoneally administered glucagon-like peptide-1 (GLP-1) involve activation of GLP-1 receptors (GLP-1R) expressed on vagal afferent fiber terminals. Central nervous system processing of GLP-1R-driven vagal afferents results in satiation signaling and enhanced insulin secretion from pancreatic-projecting vagal efferents. As the vast majority of endogenous GLP-1 is released from intestinal l-cells following ingestion, it stands to reason that paracrine GLP-1 signaling, activating adjacent GLP-1R expressed on vagal afferent fibers of gastrointestinal origin, contributes to glycemic and food intake control. However, systemic GLP-1R-mediated control of glycemia is currently attributed to endocrine action involving GLP-1R expressed in the hepatoportal bed on terminals of the common hepatic branch of the vagus (CHB). Here, we examine the hypothesis that activation of GLP-1R expressed on the CHB is not required for GLP-1's glycemic and intake suppressive effects, but rather paracrine signaling on non-CHB vagal afferents is required to mediate GLP-1's effects. Selective CHB ablation (CHBX), complete subdiaphragmatic vagal deafferentation (SDA), and surgical control rats received an oral glucose tolerance test (2.0 g glucose/kg) 10 min after an intraperitoneal injection of the GLP-1R antagonist, exendin-(9–39) (Ex-9; 0.5 mg/kg) or vehicle. CHBX and control rats showed comparable increases in blood glucose following blockade of GLP-1R by Ex-9, whereas SDA rats failed to show a GLP-1R-mediated incretin response. Furthermore, GLP-1(7–36) (0.5 mg/kg ip) produced a comparable suppression of 1-h 25% glucose intake in both CHBX and control rats, whereas intake suppression in SDA rats was blunted. These findings support the hypothesis that systemic GLP-1R mediation of glycemic control and food intake suppression involves paracrine-like signaling on GLP-1R expressed on vagal afferent fibers of gastrointestinal origin but does not require the CHB.
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Rynkiewicz, Andrzej. "Attentive Perception Can Diminish Vagal Inhibition." Journal of Psychophysiology 20, no. 1 (2006): 52–58. http://dx.doi.org/10.1027/0269-8803.20.1.52.
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A systematic decrease in heart rate when anticipating an important stimulus or when preparing to react is called anticipatory bradycardia. Numerous studies have shown that the initiation of motor activity prompts the termination of anticipatory bradycardia in reaction time tasks. However, in experiments with procedures based on more complex reactions, the termination of anticipatory bradycardia is delayed until later cardiac cycles. This unexpected effect may be attributed to perceptual processes that are engaged in the feedback mechanism essential for effectiveness in prolonged and complex motor reactions. The experiment presented in this article was carried out to verify the hypothesis that the initiation of a motor reaction, when processed simultaneously with sustained attentive perception, does not evoke acceleration of heart rate. The experimental task was a simulated shooting at a moving target. The procedure in the experimental group induced participants to attentively observe events before and after the required reaction, whereas in the control group, attentive perception of task events after the reaction was not possible. The expected pattern of heart-rate changes appeared in the experimental group. During the initial block of trials, the initiation of the motor reaction did not evoke immediate termination of anticipatory bradycardia. During later trials in the experimental group and during all trials in the control group, heart-rate changes were completely typical - heart rate increased after the motor reaction began. The results show that attentive perception engaged immediately after the initiation of motor activity can affect the pattern of phasic heart-rate changes observed during typical reaction time tasks. Additionally, the difference between the patterns characteristic of the initial and later trials suggests possible competition between the neuronal influences that modulate heart rate.