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Journal articles on the topic 'Vagal complex'

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Published: 12 October 2024

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1

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 (September 1, 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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2

Becker, L. E., and W. Zhang. "Vagal Nerve Complex in Normal Development and Sudden Infant Death Syndrome." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 23, no. 1 (February 1996): 24–33. http://dx.doi.org/10.1017/s0317167100039147.

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ABSTRACT:Background:Although the pathogenesis of sudden infant death syndrome (SIDS) is not understood, one of the major hypotheses is that a subtle defect in respiratory circuitry is an important underlying factor. The vagus nerve is a critical component of respiratory control, but its neuroanatomic complexity has limited its investigation in human disease.Methods:Correlating developmental studies on different parts of the vagus nerve allows a more comprehensive assessment of its maturation process. Comparison of the normal developing vagus nerve with nerves examined in SIDS patients suggests alterations in the nucleus tractus solitarius and dorsal vagal nucleus as well as in the peripheral vagus nerve.Results and Conclusions:The persistence of dendritic spines and lack of appropriate axonal growth implies delays in vagal maturation. Since nodose ganglia can be examined in vitro from autopsy material, perturbation to this system can be explored to evaluate further the mechanism involved in terminal vagal maturation. Although the reason for the delayed vagal maturation in SIDS is not apparent, the presence of astrogliosis in the region of the vagal nuclei is consistent with an exposure to hypoxic-ischemic events some time before death.
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3

Taché, Y., H. Yang, and H. Kaneko. "Caudal raphe-dorsal vagal complex peptidergic projections: Role in gastric vagal control." Peptides 16, no. 3 (January 1995): 431–35. http://dx.doi.org/10.1016/0196-9781(94)00212-o.

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4

Lorincz, I., E. Varga, Z. Szabó, ZS Karanyi, and ZS Varga. "Complex management of neurocardiogenic (vaso-vagal) syNcope." EP Europace 2, Supplement_1 (January 2001): A80. http://dx.doi.org/10.1016/eupace/2.supplement_1.a80-c.

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5

Rusetsky, I. I. "0 trigemino-vagal reflex." Kazan medical journal 18, no. 2 (September 23, 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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6

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 (January 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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7

Vavaiya, Kamlesh V., Sachin A. Paranjape, Gopal D. Patil, and Karen P. Briski. "Vagal complex monocarboxylate transporter-2 expression during hypoglycemia." NeuroReport 17, no. 10 (July 2006): 1023–26. http://dx.doi.org/10.1097/01.wnr.0000224766.07702.51.

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8

Poole, Sarah L., David I. Lewis, and Susan A. Deuchars. "Histamine depolarizes neurons in the dorsal vagal complex." Neuroscience Letters 432, no. 1 (February 2008): 19–24. http://dx.doi.org/10.1016/j.neulet.2007.11.055.

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9

Parain, Dominique, Marie J. Penniello, Patrick Berquen, Thierry Delangre, Catherine Billard, and Jerome V. Murphy. "Vagal nerve stimulation in tuberous sclerosis complex patients." Pediatric Neurology 25, no. 3 (September 2001): 213–16. http://dx.doi.org/10.1016/s0887-8994(01)00312-5.

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10

Hornby, Pamela J. "II. Excitatory amino acid receptors in the brain-gut axis." American Journal of Physiology-Gastrointestinal and Liver Physiology 280, no. 6 (June 1, 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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11

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 (September 1, 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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12

Varanasi, Sridhar, Jinhan Chi, and Robert L. Stephens. "Methiothepin attenuates gastric secretion and motility effects of vagal stimulants at the dorsal vagal complex." European Journal of Pharmacology 436, no. 1-2 (February 2002): 67–73. http://dx.doi.org/10.1016/s0014-2999(01)01579-5.

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13

Peters, James H., Zachary R. Gallaher, Vitaly Ryu, and Krzysztof Czaja. "Withdrawal and restoration of central vagal afferents within the dorsal vagal complex following subdiaphragmatic vagotomy." Journal of Comparative Neurology 521, no. 15 (August 23, 2013): 3584–99. http://dx.doi.org/10.1002/cne.23374.

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14

Powley, Terry L. "Brain-gut communication: vagovagal reflexes interconnect the two “brains”." American Journal of Physiology-Gastrointestinal and Liver Physiology 321, no. 5 (November 1, 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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15

Dusi, Veronica, and Gaetano Maria De Ferrari. "Vagal stimulation in heart failure." Herz 46, no. 6 (October 30, 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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16

Valenza, Gaetano, Luca Passamonti, Andrea Duggento, Nicola Toschi, and Riccardo Barbieri. "Uncovering complex central autonomic networks at rest: a functional magnetic resonance imaging study on complex cardiovascular oscillations." Journal of The Royal Society Interface 17, no. 164 (March 2020): 20190878. http://dx.doi.org/10.1098/rsif.2019.0878.

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This study aims to uncover brain areas that are functionally linked to complex cardiovascular oscillations in resting-state conditions. Multi-session functional magnetic resonance imaging (fMRI) and cardiovascular data were gathered from 34 healthy volunteers recruited within the human connectome project (the ‘100-unrelated subjects' release). Group-wise multi-level fMRI analyses in conjunction with complex instantaneous heartbeat correlates (entropy and Lyapunov exponent) revealed the existence of a specialized brain network, i.e. a complex central autonomic network (CCAN), reflecting what we refer to as complex autonomic control of the heart. Our results reveal CCAN areas comprised the paracingulate and cingulate gyri, temporal gyrus, frontal orbital cortex, planum temporale, temporal fusiform, superior and middle frontal gyri, lateral occipital cortex, angular gyrus, precuneous cortex, frontal pole, intracalcarine and supracalcarine cortices, parahippocampal gyrus and left hippocampus. The CCAN visible at rest does not include the insular cortex, thalamus, putamen, amygdala and right caudate, which are classical CAN regions peculiar to sympatho-vagal control. Our results also suggest that the CCAN is mainly involved in complex vagal control mechanisms, with possible links with emotional processing networks.
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17

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 (January 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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18

McTigue, D. M., N. K. Edwards, and R. C. Rogers. "Pancreatic polypeptide in dorsal vagal complex stimulates gastric acid secretion and motility in rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 265, no. 6 (December 1, 1993): G1169—G1176. http://dx.doi.org/10.1152/ajpgi.1993.265.6.g1169.

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High concentrations of receptors for pancreatic polypeptide (PP), a pancreatic hormone, were recently discovered in the dorsomedial region of the dorsal vagal complex (DVC). We hypothesized that gastric acid secretion and motility, digestive functions strongly influenced by vagovagal reflexes organized within the DVC, would be affected by PP applied directly to this vagal sensorimotor integration area. After urethan-anesthetized rats were prepared for antral motility recording or titrometric analysis of gastric acid output, phosphate-buffered saline or various doses of PP in phosphate-buffered saline were micropressure injected into the medial DVC. Injections of PP into the DVC produced significant, long-lasting, and dose-dependent increases in gastric acid secretion and antral motility. These gastric responses were blocked by bilateral cervical vagotomy and by atropine, suggesting that intramedullary PP stimulates vagal cholinergic pathways, resulting in enhanced gastric functions. Because PP is not synthesized within the central nervous system, these results point to a new mechanism whereby the digestive tract may modulate its own autonomic control: direct humoral action on vagovagal reflex circuits within the brain stem.
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19

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 (February 1, 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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20

Stephens, R. L., T. Ishikawa, H. Weiner, D. Novin, and Y. Tache. "TRH analogue, RX 77368, injected into dorsal vagal complex stimulates gastric secretion in rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 254, no. 5 (May 1, 1988): G639—G643. http://dx.doi.org/10.1152/ajpgi.1988.254.5.g639.

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Medullary sites inducing gastric acid secretion in response to microinjection of the stable analogue of thyrotropin-releasing hormone (TRH; RX 77368, pGlu-His-[3,3'-dimethyl]-Pro-NH2) were investigated in urethan-anesthetized rats. Gastric acid output was recorded every 2 min through a double gastric cannula constantly perfused with 0.9% saline solution maintained at pH 5.5 using an automatic titrator. Unilateral microinjection of RX 77368 (10-100 ng in 50-nl volume) into the dorsal vagal complex (DVC), the dorsal vagal nucleus and nucleus tractus solitarius, induced a significant dose-dependent stimulation of gastric acid secretion. The peak response occurred within 50 min and lasted over 1 h. Other medullary sites, including the lateral, dorsal, and parvocellular reticular nuclei; the medial longitudinal fasciculus; and the medial cuneate nucleus injected with RX 77368 (10-100 ng), were inactive. The TRH metabolites, TRH-OH and His-Pro diketopiperazine (100 ng), injected into the DVC did not influence gastric acid secretion. The stimulation of gastric acid secretion induced by DVC injection of TRH was abolished by vagotomy. These results demonstrate that 1) the DVC is an important site of action for TRH-induced stimulation of gastric acid secretion, 2) TRH action in the DVC is not secondary to the formation of TRH metabolites, and 3) the effect is expressed by vagal efferent pathways. These findings added to the high concentration of TRH-immunoreactivity and receptors in the DVC suggest a role for endogenous TRH in the regulation of vagal outflow to the stomach.
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21

Hornby, Pamela J., Carmel M. McDermott, and Vyeka Sethi. "Neurochemical organization of the dorsal vagal complex in mice." Gastroenterology 118, no. 4 (April 2000): A1176. http://dx.doi.org/10.1016/s0016-5085(00)80530-2.

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22

Abraham, Mona A., Beatrice M. Filippi, Gil Myoung Kang, Min-Seon Kim, and Tony K. T. Lam. "Insulin action in the hypothalamus and dorsal vagal complex." Experimental Physiology 99, no. 9 (September 1, 2014): 1104–9. http://dx.doi.org/10.1113/expphysiol.2014.079962.

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23

Cassell, M. D., L. Roberts, and W. T. Talman. "Glycine-containing terminals in the rat dorsal vagal complex." Neuroscience 50, no. 4 (October 1992): 907–20. http://dx.doi.org/10.1016/0306-4522(92)90214-m.

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24

Tan, Zhenjun, Ronald Fogel, Chunhui Jiang, and Xueguo Zhang. "Galanin Inhibits Gut-Related Vagal Neurons in Rats." Journal of Neurophysiology 91, no. 5 (May 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 (May 1, 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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Hernandez, E. J., D. C. Whitcomb, S. R. Vigna, and I. L. Taylor. "Saturable binding of circulating peptide YY in the dorsal vagal complex of rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 266, no. 3 (March 1, 1994): G511—G516. http://dx.doi.org/10.1152/ajpgi.1994.266.3.g511.

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The rationale for this study was to test the hypothesis that peripherally released peptide YY (PYY) acts in the vagal nuclear complex of the medulla oblongata to modulate vagal tone centrally. The objective was to determine whether circulating PYY gains access to and binds to the receptors identified in the dorsal vagal complex (DVC) under physiological conditions. Specific brain regions were microdissected after intravenous 125I-labeled PYY and 131I-labeled bovine serum albumin infusions to determine saturable accumulation of PYY in the brain and to determine if there were changes in plasma volume with large PYY infusions. Significant (P < 0.05) saturable binding was observed in the region of the brain stem containing the DVC and the pituitary. There were no significant changes in plasma volume in any region after the infusion of the excess nonradioactive PYY. We conclude that under physiological conditions circulating PYY binds to sites in the pituitary and portions of the DVC that have PYY receptors and an incomplete blood-brain barrier but does not bind to other areas that have an intact blood-brain barrier. Therefore this peripheral hormone may act centrally to modulate the digestive system and is a member of a novel class of gut hormones that function as central neuromodulators.
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27

Chen, S. L., X. Y. Wu, Z. J. Cao, J. Fan, M. Wang, C. Owyang, and Y. Li. "Subdiaphragmatic vagal afferent nerves modulate visceral pain." American Journal of Physiology-Gastrointestinal and Liver Physiology 294, no. 6 (June 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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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 (October 1, 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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29

Jacobson, Carol. "Narrow QRS Complex Tachycardias." AACN Advanced Critical Care 18, no. 3 (July 1, 2007): 264–74. http://dx.doi.org/10.4037/15597768-2007-3005.

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Narrow QRS complex tachycardias are either atrioventricular (AV) nodal passive or AV nodal active. AV nodal passive tachycardias do not require the participation of the AV node in maintenance of the tachycardia. Examples are atrial tachycardia, atrial flutter, and atrial fibrillation. Treatment is directed at ventricular rate control with calcium channel blockers or β-blockers. AV nodal active tachycardias require active participation of the AV node in maintaining the tachycardia. Examples include AV nodal reentry tachycardia and circus movement tachycardia using an accessory pathway. Treatment with a vagal maneuver or adenosine usually terminates the tachycardia. Recognition of these tachycardias is reviewed.
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30

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 (March 1, 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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31

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 (January 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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32

Cui, Cui, Fang Yu, Suqing Yin, Yuting Yang, Yingfu Jiao, Chiwai Cheung, Xiaomin Wang, et al. "Remifentanil Preconditioning Attenuates Hepatic Ischemia-Reperfusion Injury in Rats via Neuronal Activation in Dorsal Vagal Complex." Mediators of Inflammation 2018 (2018): 1–10. http://dx.doi.org/10.1155/2018/3260256.

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Remifentanil, an ultra-short acting opiate, has been reported to protect against hepatic ischemia-reperfusion injury, which is a major cause of postoperative liver dysfunction. The objective of this study was to determine whether a central vagal pathway is involved in this protective procedure. Rat models of hepatic ischemia-reperfusion were used in the experimental procedures. The results revealed that intravenous pretreatment with remifentanil decreased serum aminotransferases and hepatic histologic damage; however, an intraperitoneal injection of μ-opioid receptor antagonist did not abolish the protection of remifentanil preconditioning. c-Fos immunofluorescence of the brain stem showed that dorsal motor nucleus of the vagus was activated after remifentanil preconditioning. Moreover, serum alanine aminotransferase, histopathologic damage, and apoptosis decreased in remifentanil preconditioning group compared to vagotomized animals with remifentanil preconditioning, and there was no statistical difference of TNF-α and IL-6 between NS/Va and RPC/Va groups. In addition, remifentanil microinjection into dorsal vagal complex decreased serum aminotransferases, inflammatory cytokines, and hepatic histologic injury and apoptosis, and these effects were also abolished by a peripheral hepatic vagotomy. In conclusion, remifentanil preconditioning conferred liver protection against ischemia-reperfusion injury, which was mediated by the central vagal pathway.
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33

Boissonade, F. M., K. A. Sharkey, and J. S. Davison. "Fos expression in ferret dorsal vagal complex after peripheral emetic stimuli." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 266, no. 4 (April 1, 1994): R1118—R1126. http://dx.doi.org/10.1152/ajpregu.1994.266.4.r1118.

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The aim of this study was to investigate neuronal activation in the dorsal vagal complex of the halothane-anesthetized ferret after peripheral emetic stimuli. Neuronal activity was studied by examining the distribution of the nuclear phosphoprotein Fos using immunohistochemistry. The emetic stimuli used were electrical stimulation of the supradiaphragmatic vagal communicating branch (SVCB) or intraduodenal injection of hypertonic saline. Electrical stimulation of the SVCB induced the densest Fos expression within the medial subnucleus of the nucleus of the solitary tract. After hypertonic saline injection, the greatest density of Fos-positive nuclei was observed within the area postrema and also in the medial subnucleus of the nucleus of the solitary tract. It was concluded that the emetic response to hypertonic saline involves neurons in both the area postrema and the nucleus of the solitary tract, especially the medial subnucleus, and that the medial subnucleus is important in the emetic response to SVCB stimulation.
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34

Ekmekçi, Hakan, and Hülagu Kaptan. "Vagal Nerve Stimulation." Open Access Macedonian Journal of Medical Sciences 5, no. 3 (May 7, 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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35

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 (November 1, 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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36

Yang, H., G. Ohning, and Y. Tache. "TRH in dorsal vagal complex mediates acid response to excitation of raphe pallidus neurons in rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 265, no. 5 (November 1, 1993): G880—G886. http://dx.doi.org/10.1152/ajpgi.1993.265.5.g880.

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The role of thyrotropin-releasing hormone (TRH) in the dorsal vagal complex (DVC) in the acid response to excitation of raphe pallidus neurons was investigated in urethan-anesthetized rats with gastric fistula. Kainic acid (0.19 microgram/30 nl) microinjected into the raphe pallidus stimulated gastric acid secretion. The response was prevented by vagotomy. A specific polyclonal TRH antibody, 8964, was raised and characterized (50% inhibitory dose for TRH was 80 pg/ml at an antibody final dilution of 1:10(5)). The TRH antibody injected intracisternally blocked the acid response to intracisternal TRH, but not that of the TRH analogue RX-77368. The TRH antibody (0.33, 0.65, or 1.3 micrograms.100 nl-1.site-1) microinjected bilaterally into the DVC prevented dose dependently by 31, 60, and 76%, respectively, the increase in acid secretion induced by kainic acid injected into the raphe pallidus. The TRH antibody (1.3 microgram/site) microinjected into medullary sites outside of the DVC had no effect. These data indicate that excitation of raphe pallidus neurons induces a vagal-dependent stimulation of gastric acid secretion that is mediated by endogenous TRH in the DVC. TRH neurons in the raphe pallidus projecting to the DVC may have a physiological relevance in the vagal regulation of gastric function.
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37

Tanaka, Toshiyuki, Luke H. VanKlompenberg, and Michael G. Sarr. "Selective role of vagal and non-vagal innervation in control of migrating motor complex (MMC) and postprandial motility." Gastroenterology 118, no. 4 (April 2000): A1050. http://dx.doi.org/10.1016/s0016-5085(00)86351-9.

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38

Taché, Y., H. Yang, and M. Yoneda. "Vagal Regulation of Gastric Function Involves Thyrotropin Releasing Hormone in the Medullary Raphe Nuclei and Dorsal Vagal Complex." Digestion 54, no. 2 (1993): 65–72. http://dx.doi.org/10.1159/000201015.

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39

Sawai, Setsu, Ryuji Sakakibara, Kazuaki Kanai, Naoki Kawaguchi, Tomoyuki Uchiyama, Tatsuya Yamamoto, Takashi Ito, Zhi Liu, and Takamichi Hattori. "Isolated Vomiting due to a Unilateral Dorsal Vagal Complex Lesion." European Neurology 56, no. 4 (2006): 246–48. http://dx.doi.org/10.1159/000096673.

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40

McCann, M. J., and R. C. Rogers. "Oxytocin excites gastric-related neurones in rat dorsal vagal complex." Journal of Physiology 428, no. 1 (September 1, 1990): 95–108. http://dx.doi.org/10.1113/jphysiol.1990.sp018202.

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41

Glatzer, Nicholas R., Andrei V. Derbenev, Bruce W. Banfield, and Bret N. Smith. "Endomorphin-1 Modulates Intrinsic Inhibition in the Dorsal Vagal Complex." Journal of Neurophysiology 98, no. 3 (September 2007): 1591–99. http://dx.doi.org/10.1152/jn.00336.2007.

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Mu-opioid receptor (MOR) agonists profoundly influence digestive and other autonomic functions by modulating neurons in nucleus tractus solitarius (NTS) and dorsal motor nucleus of the vagus (DMV). Whole cell recordings were made from NTS and DMV neurons in brain stem slices from rats and transgenic mice that expressed enhanced green fluorescent protein (EGFP) under the control of a GAD67 promoter (EGFP-GABA neurons) to identify opioid-mediated effects on GABAergic circuitry. Synaptic and membrane properties of EGFP-GABA neurons were assessed. The endogenous selective MOR agonist endomorphin-1 (EM-1) reduced spontaneous and evoked excitatory postsynaptic currents (EPSCs) and inhibitory postsynaptic currents (IPSCs) in both rat and mouse DMV neurons. Electrical stimulation of the solitary tract evoked constant-latency EPSCs in ∼50% of EGFP-GABA neurons, and the responses were reduced by EM-1 application. EM-1 reduced action potential firing, the frequency and amplitude of synaptic inputs in EGFP-GABA neurons and responses to direct glutamate stimulation. A subset of EGFP-GABA neurons colocalized mRFP1 after retrograde, transneuronal infection after gastric inoculation with PRV-614, indicating that they synapsed with gastric-projecting DMV neurons. Glutamate photolysis stimulation of intact NTS projections evoked IPSCs in DMV neurons, and EM-1 reduced the evoked response, most likely by activation of MOR on the soma of premotor GABA neurons in NTS. Naltrexone or H-d-Phe-Cys-Tyr-d-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP), MOR antagonists, blocked the effects of EM-1. Our results show that GABA neurons in the NTS receive direct vagal afferent input and project to gastric-related DMV neurons. Furthermore, modulation by EM-1 of specific components of the vagal complex differentially suppresses excitatory and inhibitory synaptic input to the DMV by acting at different receptor locations.
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42

Lang, Ivan M., Caron Dean, Bidyut K. Medda, and Reza Shaker. "Functional mapping of phases of swallowing in dorsal vagal complex." Gastroenterology 118, no. 4 (April 2000): A1184. http://dx.doi.org/10.1016/s0016-5085(00)80562-4.

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43

Fodor, Mariann, Csilla Pammer, Tamás Görcs, and Miklós Palkovits. "Neuropeptides in the human dorsal vagal complex: An immunohistochemical study." Journal of Chemical Neuroanatomy 7, no. 3 (August 1994): 141–57. http://dx.doi.org/10.1016/0891-0618(94)90025-6.

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44

McTigue, D. M., G. E. Hermann, and R. C. Rogers. "Effect of pancreatic polypeptide on rat dorsal vagal complex neurons." Journal of Physiology 499, no. 2 (March 1, 1997): 475–83. http://dx.doi.org/10.1113/jphysiol.1997.sp021942.

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45

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 (August 1, 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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46

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 (September 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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47

Emch, Gregory S., Gerlinda E. Hermann, and Richard C. Rogers. "TNF-α activates solitary nucleus neurons responsive to gastric distension." American Journal of Physiology-Gastrointestinal and Liver Physiology 279, no. 3 (September 1, 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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48

Mönnikes, Hubert, Gerd Lauer, Christoph Bauer, Johannes Tebbe, Tillmann T. Zittel, and Rudolf Arnold. "Pathways of Fos expression in locus ceruleus, dorsal vagal complex, and PVN in response to intestinal lipid." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 273, no. 6 (December 1, 1997): R2059—R2071. http://dx.doi.org/10.1152/ajpregu.1997.273.6.r2059.

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Exogenous cholecystokinin (CCK) injected peripherally mimics effects of lipid entering the intestine on food intake and gastric motility via vagal afferents and induces c- fos expression in the locus ceruleus complex (LCC), nucleus of the solitary tract (NTS), area postrema (AP), and paraventricular nucleus (PVN). However, the role of peripheral endogenous CCK in induction of c- fos expression in the brain at ingestion of nutrients is controversial. In awake rats, intraduodenal lipid infusion markedly increased Fos protein-like immunoreactivity (FLI) in these brain nuclei. Perivagal capsaicin pretreatment reduced the increase of FLI in the LCC, NTS, and PVN by 66–86% and in the AP by 46%. The CCK-A receptor antagonist MK-329 (0.1 mg/kg ip) diminished the FLI increase in LC, NTS, AP, and PVN by 39–100%; the CCK-B receptor antagonist L-365,260 reduced the increased FLI in the AP by 54%. After capsaicin pretreatment, both CCK antagonists had additional inhibitory effects only on FLI in the AP. These findings suggest that entry of lipid into the intestine activates c- fos in the LCC, NTS, and PVN predominantly via CCK-A receptors on vagal afferents and in the AP via vagal and nonvagal pathways, as well as CCK-B and CCK-A receptors.
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49

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 (September 1, 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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50

Rynkiewicz, Andrzej. "Attentive Perception Can Diminish Vagal Inhibition." Journal of Psychophysiology 20, no. 1 (January 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.
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