Disease relevance of Vagus Nerve

• Ventricular asystole during vagus nerve stimulation for epilepsy in humans [1].
• The present review aims to describe the role of 5-HT in anticancer drug-induced emesis from the viewpoint of 5-HT release and afferent vagus nerve activity [2].
• Three to five days after pre-treatment of the cervical vagus nerves with capsaicin, phenyldiguanidine and veratrine given intravenously invariably evoked bradycardia, hypotension and apnoea, while the reflex responses to intravenous injection of capsaicin and some of its pungent congeners were greatly reduced or even abolished [3].
• Right coronary occlusion in animals with intact and sectioned vagus nerves evoked noradrenaline and adrenaline release that was significantly correlated with a fall in arterial pressure [4].
• RESULTS: Initial cytokine release during septic peritonitis was enhanced after previous vagotomy and was decreased after nicotine pretreatment, independently of the integrity of the vagus nerve [5].

Psychiatry related information on Vagus Nerve

• Chronic vagus nerve stimulation improves alertness and reduces rapid eye movement sleep in patients affected by refractory epilepsy [6].
• Electroconvulsive therapy can also be used safely in people with epilepsy, and vagus nerve stimulation may have some utility in the treatment of depressive disorders as well [7].
• We conclude that, in vivo, intraperitoneal LPS lowers visceral pain threshold (allodynia) through a mechanism involving mast cell degranulation and IL-1beta and TNF-alpha release and that the vagus nerve may exert a tonic protective role against LPS-induced rectal allodynia [8].
• We conclude that 1) hyperoxia-induced bradycardia in conscious dogs is mediated by efferents of the vagus nerve; 2) its afferent pathway remains unknown, but its long response time suggests mechanisms other than chemoreceptor reflexes or other known neural reflexes; and 3) it is completely reversible [9].
• Our findings strongly suggest that the inhibitory effect of PYY on gastric secretion is in part mediated by a non-vagal pathway and the inhibitory effect of PYY on gastric motor activities is completely dependent on vagal innervation, but the vagus nerve acts as an inhibitory modulator of the inhibitory effect of PYY on gastric secretion [10].

High impact information on Vagus Nerve

• Electrical stimulation of the vagus nerve inhibits TNF synthesis in wild-type mice, but fails to inhibit TNF synthesis in alpha7-deficient mice [11].
• The nervous system, through the vagus nerve, can inhibit significantly and rapidly the release of macrophage TNF, and attenuate systemic inflammatory responses [11].
• Receptors of the 5-HT3 type have been characterized on isolated peripheral tissue models such as the rat vagus nerve, guinea-pig ileum and isolated rabbit heart [12].
• The mammalian heart rate is regulated by the vagus nerve, which acts via muscarinic acetylcholine receptors to cause hyperpolarization of atrial pacemaker cells [13].
• Modulation of memory processing by cholecystokinin: dependence on the vagus nerve [14].

Chemical compound and disease context of Vagus Nerve

• To assess the effects of hyperglycemia on the neurotrophin content and transport in this system, cervical vagus nerves of streptozotocin (STZ)-induced diabetic rats were studied at 8, 16, and 24 weeks after the induction of diabetes [15].
• Hexamethonium (60 mg/kg i.v.) had no effect on the bradycardia produced by the muscarinic agonist methacholine (100-300 micrograms/kg/min i.v.). The dose of pirenzepine that blocked the neostigmine-induced bradycardia was lower than required for blocking the bradycardia produced by vagus nerve stimulation [16].
• Based on previous results obtained in whole ganglion and showing the presence of cholinergic cell bodies among the afferent fibres of the vagus nerve, this preparation was used to study choline uptake by neuron cell somata [17].
• 2. Stimulation of the preganglionic cervical vagus nerve in anaesthetized guinea-pigs, caused bronchoconstriction and bradycardia which were mimicked by an intravenous dose of ACh [18].
• The effects of electrical stimulation of the vagus nerve, a proposed treatment for patients with intractable epilepsy, on focal interictal spikes produced by penicillin and EEG secondarily generalized seizures induced by pentylenetetrazol were assessed in rats [19].

Biological context of Vagus Nerve

• In cats anesthetized with chloralose-pentobarbital and artificially ventilated, electrical stimulation of the caudal end of the cut cervical vagus nerve has a biphasic effect on the bronchoconstriction induced by an intravenous infusion of serotonin [20].
• The purpose of this investigation was 2-fold: first, to determine the velocity of peristalsis in the smooth muscle area of opossum esophagus before and after administration of atropine; second, to evaluate the role of the vagus nerves in the control of the propagative nature of esophageal peristalsis [21].
• The evidence indicates that afferent impulses via the right vagus nerve may be important under basal conditions, but they are not required for the ANP release induced by blood volume expansion [22].
• Reflex coronary vasodilation could still be evoked when myelinated nerve fibers were blocked selectively by cooling the cervical vagus nerves to 7-8 degrees C but was abolished by cooling to 0 degrees C, by cutting the pulmonary vagal branches, or by giving atropine [23].
• Association of neurotensin binding sites with sensory and visceromotor components of the vagus nerve [24].

Anatomical context of Vagus Nerve

• However, haloperidol did not block the effect of electrical stimulation of vagus nerve on body of the esophagus or the lower esophageal sphincter [25].
• METHODS: After bile duct ligation (BDL), the vagus nerve was resected; 7 days later, expression of M3 acetylcholine receptor was evaluated [26].
• Bombesin response appears to be central nervous system-mediated; its expression is not dependent on the vagus nerve or the adrenal glands, and does not rely on a decrease in gastrin secretion [27].
• It can be summarized as follows: It was shown that an increase in blood glucose concentration produced an increase in the activity of the pancreatic branch of the vagus nerve whereas it induced a decrease in the activity of the pancreatic branch of the splanchnic nerve and adrenal nerve [28].
• An isolated atrial contraction induced by administering 1 mg acetylcholine chloride into the atrioventricular node artery or by vagus nerve stimulation could produce complete valve closure [29].

Associations of Vagus Nerve with chemical compounds

• Blockade of gamma-aminobutyric acid (GABA) receptor function by direct microinjection of the GABA receptor antagonist bicuculline into the nucleus ambiguus of the brainstem produced a marked, dose-related depression of heart rate and blood pressure which was mediated by the vagus nerve [30].
• Vagus nerve firing is also stimulated by CNI-1493, a tetravalent guanylhydrazone molecule that inhibits systemic inflammation [31].
• Efferent activity in the vagus nerve can prevent endotoxin-induced shock by attenuating tumor necrosis factor (TNF) synthesis [31].
• To evaluate the role of NO in parasympathetic inhibition of the beta-adrenergic contractile response in vivo, we assessed the inotropic response to dobutamine before and during bilateral vagus nerve stimulation in closed-chest dogs [32].
• Rectal distention-induced colonic net water secretion in rats involves tachykinins, capsaicin sensory, and vagus nerves [33].

Gene context of Vagus Nerve

• Direct electrical stimulation of the peripheral vagus nerve in vivo during lethal endotoxaemia in rats inhibited TNF synthesis in liver, attenuated peak serum TNF amounts, and prevented the development of shock [34].
• Accumulation of immunoreactivity proximal to a ligature showed that mGluR were transported peripherally in the vagus nerves [35].
• Issues considered include, the effects of systemic injection of CCK on consummatory and operant feeding, the role of the vagus nerve, the effects of CCKB receptor antagonists, and the neuroendocrine responses to exogenous CCK [36].
• The motor neurites expressing R-cadherin have a different course within the brain than the sensory neurites expressing N-cadherin, although they form the common sensory/motor roots of the vagus nerve at the surface of the brain [37].
• In addition, our analyses establish Nurr1 as an early marker for the dorsal motor nucleus (DMN) of the vagus nerve [38].

Analytical, diagnostic and therapeutic context of Vagus Nerve

• Three weeks of experimental diabetes caused deficits in the accumulation of choline acetyltransferase activity proximal to 24-h constrictions in the left sciatic and vagus nerves [39].
• The authors prospectively assessed drug reduction and patient satisfaction in 21 patients using vagus nerve stimulation (VNS) for refractory epilepsy and compared results to a case-matched control group with a mean follow-up of 13.2 months [40].
• 1. A single fibre dissection technique was used to record activity from efferent fibres in the left cervical vagus nerve of urethane anaesthetized rats [41].
• Hn1 was also increased in the dorsal motor nucleus and the nucleus ambiguous after vagus nerve axotomy, another regeneration model [42].
• Perfusion of the whole guinea-pig vagus nerve with capsaicin (0.3 microM) or pH 5 buffer caused depolarization [43].

References