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Artykuły w czasopismach na temat „Vagal complex”

Autor: Grafiati

Data publikacji: 12 października 2024

Data aktualizacji: 31 lipca 2025

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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 (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

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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 (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

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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 (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 (2001): A80. http://dx.doi.org/10.1016/eupace/2.supplement_1.a80-c.

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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

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6

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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7

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 discusse

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8

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 gastrointest

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9

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 nee

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10

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 (2006): 1023–26. http://dx.doi.org/10.1097/01.wnr.0000224766.07702.51.

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11

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

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12

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 (2001): 213–16. http://dx.doi.org/10.1016/s0887-8994(01)00312-5.

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13

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 (2002): 67–73. http://dx.doi.org/10.1016/s0014-2999(01)01579-5.

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14

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 (2013): 3584–99. http://dx.doi.org/10.1002/cne.23374.

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15

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

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16

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 va

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17

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 (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

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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 (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

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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 (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 duri

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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 (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-depende

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21

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

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22

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.

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23

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)

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24

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, blo

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25

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

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26

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

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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 (2014): 1104–9. http://dx.doi.org/10.1113/expphysiol.2014.079962.

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

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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 (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 v

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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 i

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Jacobson, Carol. "Narrow QRS Complex Tachycardias." AACN Advanced Critical Care 18, no. 3 (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. Treatmen

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Cui, Cui, Fang Yu, Suqing Yin, 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

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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 affer

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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 (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 sali

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35

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 occ

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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 presente

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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 (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 intracisterna

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EkmekÃ§i, Hakan, and HÃ¼lagu 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 connectio

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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.

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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 (2000): A1050. http://dx.doi.org/10.1016/s0016-5085(00)86351-9.

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

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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 (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

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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 (2000): A1184. http://dx.doi.org/10.1016/s0016-5085(00)80562-4.

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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 (1994): 141–57. http://dx.doi.org/10.1016/0891-0618(94)90025-6.

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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 (1997): 475–83. http://dx.doi.org/10.1113/jphysiol.1997.sp021942.

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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 (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

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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 result

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Shen, Xiling. "Abstract SY09-01: Targeting the vagal gut-brain axis: A new approach to combat cachexia." Cancer Research 85, no. 8_Supplement_2 (2025): SY09–01—SY09–01. https://doi.org/10.1158/1538-7445.am2025-sy09-01.

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Abstract Cancer-associated cachexia is a complex, incurable syndrome responsible for nearly one-third of cancer-related deaths, driving therapy resistance and increasing mortality in affected patients. In this study, we identify altered vagal tone as a consequence of cancer-induced systemic inflammation in cachectic animal models. This vagal dysregulation disrupts the liver-brain vagal axis, leading to the rewiring of liver protein metabolism through the depletion of HNF4α, a key regulator of liver function. Notably, downregulation of liver HNF4α in wildtype mice induces cachectic phenotypes.

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