Osmosensitive vagal receptors in the small intestine of the cat

Mei, N.; Garnier, Lucie

doi:10.1016/0165-1838(86)90022-6

Cited by 76 publications

(33 citation statements)

References 37 publications

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“…Electrophysiological studies have shown that intragastric and enteric delivery of amino acids and lipids both activate the afferent vagus nerve as described above [31,32,33,55,56]. The intraportal administration of amino acids also activates the afferent vagus nerve [57].…”

Section: Signaling Mechanisms Of the Gut-brain Axismentioning

confidence: 99%

Biological Significance of Glutamate Signaling during Digestion of Food through the Gut-Brain Axis

Kitamura

Tsurugizawa²,

Torii³

2011

Digestion

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Monosodium L-glutamate (MSG) elicits a unique taste termed umami and is widely used as a flavor enhancer in various cuisines. In addition, recent studies suggest the existence of sensors for L-glutamate (Glu) and transduction molecules in the gut mucosa as well as in the oral cavity. The vagal gastric afferent responds specifically to the luminal stimulation of Glu in the stomach and regulates the autonomic reflexes. The intragastric infusion of Glu also activates several brain areas (insular cortex, limbic system, and hypothalamus) and is able to induce flavor-preference learning in rats. These results suggest that umami signaling via gustatory and visceral pathways plays an important role in the processes of digestion, absorption, metabolism, and other physiological functions via activation of the brain.

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Section: Signaling Mechanisms Of the Gut-brain Axismentioning

confidence: 99%

Biological Significance of Glutamate Signaling during Digestion of Food through the Gut-Brain Axis

Kitamura

Tsurugizawa²,

Torii³

2011

Digestion

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“…At the central level, microinjection of glucose into either the DMV or the NTS decreases gastric motility and secretion (24, 58, 61) although a recent study did not observe any effects on gastric relaxation following mild hyperglycemia due to intracisternal application of dextrose (79). Several studies have demonstrated that subpopulations of NTS and DMV neurons respond to alterations in glucose by either increasing or decreasing their activity (1,6,7,18,19,48,73,77,78), and we have demonstrated recently that synaptic transmission from the central nerve terminals of vagal afferent neurons is dependent upon glucose concentration (73), suggesting that the synaptic connections between vagal afferent fibers and NTS neurons are a probable site of action of glucose to modulate vagovagal reflexes.At a peripheral level, both vagal afferent neurons and nerve terminals are excited by glucose in a concentration-dependent manner (29,46,47). Although glucose appears capable of exciting vagal afferent neurons directly (29), at least part of the glucose-induced excitation of vagal afferent nerves is indirect, or paracrine, in nature.…”

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confidence: 99%

Glucose increases synaptic transmission from vagal afferent central nerve terminals via modulation of 5-HT₃ receptors

Wan

Browning²

2008

American Journal of Physiology-Gastrointestinal and Liver Physi

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Acute hyperglycemia has profound effects on vagally mediated gastrointestinal functions. We have reported recently that the release of glutamate from the central terminals of vagal afferent neurons is correlated directly with the extracellular glucose concentration. The present study was designed to test the hypothesis that 5-HT(3) receptors present on vagal afferent nerve terminals are involved in this glucose-dependent modulation of glutamatergic synaptic transmission. Whole-cell patch-clamp recordings were made from neurons of the nucleus tractus solitarius (NTS) in thin rat brainstem slices. Spontaneous and evoked glutamate release was decreased in a concentration-dependent manner by the 5-HT(3) receptor selective antagonist, ondansetron. Alterations in the extracellular glucose concentration induced parallel shifts in the ondansetron-mediated inhibition of glutamate release. The changes in excitatory synaptic transmission induced by extracellular glucose concentration were mimicked by the serotonin uptake inhibitor, fenfluramine. These data suggest that glucose alters excitatory synaptic transmission within the rat brainstem via actions on tonically active 5-HT(3) receptors, and the number of 5-HT(3) receptors on vagal afferent nerve terminals is positively correlated with the extracellular glucose concentration. These data indicate that the 5-HT(3) receptors present on synaptic connections between vagal afferent nerve terminals and NTS neurons are a strong candidate for consideration as one of the sites where glucose acts to modulate vagovagal reflexes.

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“…In fact, ingestion of glucose increases vagal afferent fiber discharge (20,30,31) and increases c-Fos expression in the dorsal vagal complex (53, 57). Furthermore, hyperglycemia enhances vagal afferent gastrointestinal sensory perception (37).…”

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confidence: 99%

d-Glucose modulates synaptic transmission from the central terminals of vagal afferent fibers

Wan¹,

Browning²

2008

American Journal of Physiology-Gastrointestinal and Liver Physi

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Wan S, Browning KN. D-Glucose modulates synaptic transmission from the central terminals of vagal afferent fibers. Am J Physiol Gastrointest Liver Physiol 294: G757-G763, 2008. First published January 17, 2008 doi:10.1152/ajpgi.00576.2007.-Experimental evidence suggests that glucose modulates gastric functions via vagally mediated effects. It is unclear whether glucose affects only peripheral vagal nerve activity or whether glucose also modulates vagal circuitry at the level of the brain stem. This study used whole cell patch-clamp recordings from neurons of the nucleus of the tractus solitarius (NTS) to assess whether acute variations in glucose modulates vagal brain stem neurocircuitry. Increasing D-glucose concentration induced a postsynaptic response in 40% of neurons; neither the response type (inward vs. outward current) nor response magnitude was altered in the presence of tetrodotoxin suggesting direct effects on the NTS neuronal membrane. In contrast, reducing D-glucose concentration induced a postsynaptic response (inward or outward current) in 54% of NTS neurons; tetrodotoxin abolished these responses, suggesting indirect sites of action. The frequency, but not amplitude, of spontaneous and miniature excitatory postsynaptic currents (EPSCs) was correlated with D-glucose concentration in 79% of neurons tested (n ϭ 48). Prior surgical afferent rhizotomy abolished the ability of D-glucose to modulate spontaneous EPSC frequency, suggesting presynaptic actions at vagal afferent nerve terminals to modulate glutamatergic synaptic transmission. In experiments in which EPSCs were evoked via electrical stimulation of the tractus solitarius, EPSC amplitude correlated with D-glucose concentration. These effects were not mimicked by L-glucose, suggesting the involvement of glucose metabolism, not uptake, in the nerve terminal. These data suggest that the synaptic connections between vagal afferent nerve terminals and NTS neurons are a strong candidate for consideration as one of the sites where glucose-evoked changes in vagovagal reflexes occurs. brain stem; electrophysiology; vagus DELAYED GASTRIC EMPTYING, or gastroparesis (diabetic gastropathy) in its extreme state, is reported in ϳ35-50% of patients with Type 1 or Type 2 diabetes (17,25,44,52) and is associated with early satiety, nausea, vomiting, and abdominal pain. Autonomic nerve dysfunction(s) undoubtedly contribute to the development of this syndrome (52), but reports that physiological hyperglycemia delays gastric emptying have led to the understanding that poor glycemic control per se may be responsible for at least some of these symptoms (25,26,37,38,45). Acute changes in blood glucose concentration, even within the physiological range, have profound effects on gastrointestinal functions, including gastric emptying. In healthy subjects, gastric emptying of both solids and liquids is slower at a blood glucose concentration of 8 mM than at 4 mM, and profound hyperglycemia (15 mM) causes a clear relaxation of the proximal stomach (29, 37). Hypoglycemia,...

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Osmosensitive vagal receptors in the small intestine of the cat

Cited by 76 publications

References 37 publications

Biological Significance of Glutamate Signaling during Digestion of Food through the Gut-Brain Axis

Biological Significance of Glutamate Signaling during Digestion of Food through the Gut-Brain Axis

Glucose increases synaptic transmission from vagal afferent central nerve terminals via modulation of 5-HT₃ receptors

d-Glucose modulates synaptic transmission from the central terminals of vagal afferent fibers

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Osmosensitive vagal receptors in the small intestine of the cat

Cited by 76 publications

References 37 publications

Biological Significance of Glutamate Signaling during Digestion of Food through the Gut-Brain Axis

Biological Significance of Glutamate Signaling during Digestion of Food through the Gut-Brain Axis

Glucose increases synaptic transmission from vagal afferent central nerve terminals via modulation of 5-HT3 receptors

d-Glucose modulates synaptic transmission from the central terminals of vagal afferent fibers

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Glucose increases synaptic transmission from vagal afferent central nerve terminals via modulation of 5-HT₃ receptors