d-Glucose anomers in the nucleus of the vagus nerve can depress gastric motility of rats

Takeo, Satoshi; Ohtake, Masahiro; Yamazaki, Masatoshi

doi:10.1016/0006-8993(85)90611-0

Cited by 11 publications

(8 citation statements)

References 10 publications

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“…These investigators demonstrated a prominent action of glucose to increase vagal afferent excitatory synaptic transmission to NTS neurons. Sakaguchi et al (31,32) reported that glucose injection into the dorsal motor nucleus of the vagus of anesthetized rats decreases gastric motility. In addition, Ferreira et al (11) demonstrated that administration of glucose into the nucleus tractus solitarius modulates gastric motor and secretory functions.…”

Section: Discussionmentioning

confidence: 99%

Gastric relaxation induced by hyperglycemia is mediated by vagal afferent pathways in the rat

Zhou

Owyang³

2008

American Journal of Physiology-Gastrointestinal and Liver Physi

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Hyperglycemia has a profound effect on gastric motility. However, little is known about the site and mechanism that sense alteration in blood glucose level. The identification of glucose-sensing neurons in the nodose ganglia led us to hypothesize that hyperglycemia acts through vagal afferent pathways to inhibit gastric motility. With the use of a glucose-clamp rat model, we showed that glucose decreased intragastric pressure in a dose-dependent manner. In contrast to intravenous infusion of glucose, intracisternal injection of glucose at 250 and 500 mg/dl had little effect on intragastric pressure. Pretreatment with hexamethonium, as well as truncal vagotomy, abolished the gastric motor responses to hyperglycemia (250 mg/dl), and perivagal and gastroduodenal applications of capsaicin significantly reduced the gastric responses to hyperglycemia. In contrast, hyperglycemia had no effect on the gastric contraction induced by electrical field stimulation or carbachol (10(-5) M). To rule out involvement of serotonergic pathways, we showed that neither granisetron (5-HT(3) antagonist, 0.5 g/kg) nor pharmacological depletion of 5-HT using p-chlorophenylalanine (5-HT synthesis inhibitor) affected gastric relaxation induced by hyperglycemia. Lastly, N(G)-nitro-L-arginine methyl ester (L-NAME) and a VIP antagonist each partially reduced gastric relaxation induced by hyperglycemia and, in combination, completely abolished gastric responses. In conclusion, hyperglycemia inhibits gastric motility through a capsaicin-sensitive vagal afferent pathway originating from the gastroduodenal mucosa. Hyperglycemia stimulates vagal afferents, which, in turn, activate vagal efferent cholinergic pathways synapsing with intragastric nitric oxide- and VIP-containing neurons to mediate gastric relaxation.

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Section: Discussionmentioning

confidence: 99%

Gastric relaxation induced by hyperglycemia is mediated by vagal afferent pathways in the rat

Zhou

Owyang³

2008

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…The starting point in these studies was to assess whether microinjection of d ‐glucose into the DMV of anaesthetized rats would decrease intragastric pressure and inhibit gastric motility. Our rationale for pursuing these experiments was based on the findings of Sakaguchi & colleagues, who reported that microinjection of d ‐glucose into the DMV can depress gastric motility of rats (Sakaguchi et al 1985, 1994).…”

Section: Discussionmentioning

confidence: 99%

“…Neurones in both NTS and DMV have also been shown to be affected by glucose. Glucose injected into the DMV of anaesthetized rats has been shown to decrease gastric motility and intragastric pressure (Sakaguchi et al 1985, 1994). Conversely, gastric motility or pressure did not seem to be affected when glucose was injected into the NTS, although additional studies indicated that glucose injected into the NTS could reduce gastric acid secretion (Sakaguchi & Sato, 1987).…”

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confidence: 99%

Glucose effects on gastric motility and tone evoked from the rat dorsal vagal complex

Ferreira

Browning

Sahibzada

et al. 2001

The Journal of Physiology

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1. To examine the effects of glucose on the central components of the vago-vagal reflex control of gastric function, we performed both in vivo and in vitro experiments on neurones in the medial nucleus of the tractus solitarius (mNTS) and in the dorsal motor nucleus of the vagus (DMV).2. In the in vivo anaesthetized rat preparation, unilateral microinjection of D-glucose (10 or 50 mM (60 nl) _1) in mNTS produced inhibition of gastric motility and an increase in intragastric pressure. D-glucose had no effect in the DMV.3. In the in vitro rat brainstem slice preparation, whole-cell recordings of DMV neurones showed that increasing the glucose concentration of the perfusion solution from 5 mM to 15 or 30 mM produced outward currents of 35 ± 5 pA (n = 7) and 51 ± 10 pA (n = 11), respectively. These were blocked by tetrodotoxin and picrotoxin, indicating that glucose was acting indirectly to cause the release of GABA. Decreasing the glucose concentration of the perfusing solution by one-half produced an inward current of 36 ± 5 pA (n = 7).4. Stimulation of the NTS evoked inhibitory postsynaptic currents (IPSCs) in DMV neurones. The amplitude of the evoked IPSCs was positively correlated with glucose concentration. Perfusion with the ATP-sensitive K + (K ATP ) channel opener diazoxide mimicked the effect of reduced glucose, while perfusion with the K ATP channel blocker glibenclamide mimicked the effects of increased glucose. 5. Our data indicate that glucose had no direct excitatory effect on DMV neurones, but DMV neurones appear to be affected by an action of glucose on cell bodies of mNTS neurones via effects on an ATP-sensitive potassium channel.Journal of Physiology (2001), 536.1, pp.141-152 12276 141 project to the parasympathetic ganglia and the enteric ganglia innervating the digestive tract (Rogers et al. 1995). Most of the projections from the NTS to the DMV appear to be inhibitory (McCann & Rogers, 1994) and, although the neurotransmitter released is unknown, indirect evidence suggests that it is GABA (Feng et al. 1990;Travagli et al. 1991;Washaban et al. 1995;Sivarao et al. 1998;.Glucose exerts pronounced effects both on vagal sensory nerves and on central components of the reflexes. The hepatic portal area appears to have glucose sensors linked to hepatic vagal afferent nerves (Sakaguchi & Shimojo, 1984;Sakaguchi et al. 1994). In fact, glucose administered into the hepatic portal vein has been reported to decrease hepatic vagal afferent discharge rate (Niijima, 1969;Niijima & Mequid, 1994). Neurones in both NTS and DMV have also been shown to be affected by glucose. Glucose injected into the DMV of anaesthetized rats has been shown to decrease gastric motility and intragastric pressure (Sakaguchi et al. 1985(Sakaguchi et al. , 1994. Conversely, gastric motility or pressure did not seem to be affected when glucose was injected into the NTS, although additional studies indicated that glucose injected into the NTS could reduce gastric acid secretion (Sakaguchi & Sato, 1987).Electrophysiological studie...

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“…Research suggests that acute hyperglycaemia affects a subpopulation of neurons in the nucleus tractus solitarii (NTS) and dorsal motor nucleus of the vagus (DMV) (Mizuno & Oomura, 1984; Kobashi & Adachi, 1994; Ferreira et al 2001; Balfour et al 2006). Several investigators have shown that glucose injection into the DMV of anaesthetized rats decreases gastric motility (Sakaguchi et al 1985). Ferreira et al (2001) demonstrated that glucose administration into the NTS modulates gastric motor function.…”

Section: Introductionmentioning

confidence: 99%

Electrophysiological identification of glucose-sensing neurons in rat nodose ganglia

Grabauskas

Song

Zhou

et al. 2010

The Journal of Physiology

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The vagal afferent system is strategically positioned to mediate rapid changes in motility and satiety in response to systemic glucose levels. In the present study we aimed to identify glucose-excited and glucose-inhibited neurons in nodose ganglia and characterize their glucose-sensing properties. Whole-cell patch-clamp recordings in vagal afferent neurons isolated from rat nodose ganglia demonstrated that 31/118 (26%) neurons were depolarized after increasing extracellular glucose from 5 to 15 mm; 19/118 (16%) were hyperpolarized, and 68/118 were non-responsive. A higher incidence of excitatory response to glucose occurred in gastric-than in portal vein-projecting neurons, the latter having a higher incidence of inhibitory response. In glucose-excited neurons, elevated glucose evoked membrane depolarization (11 mV) and an increase in membrane input resistance (361 to 437 M ). Current reversed at −99 mV. In glucose-inhibited neurons, membrane hyperpolarization (−13 mV) was associated with decreased membrane input resistance (383 to 293 M ). Current reversed at −97 mV. Superfusion of tolbutamide, a K ATP channel sulfonylurea receptor blocker, elicited identical glucose-excitatory but not glucose-inhibitory responses. Kir6.2 shRNA transfection abolished glucose-excited but not glucose-inhibited responses. Phosphatidylinositol bisphosphate (PIP 2 ) depletion using wortmannin increased the fraction of glucose-excited neurons from 26% to 80%. These results show that rat nodose ganglia have glucose-excited and glucose-inhibited neurons, differentially distributed among gastric-and portal vein-projecting nodose neurons. In glucose-excited neurons, glucose metabolism leads to K ATP channel closure, triggering membrane depolarization, whereas in glucose-inhibited neurons, the inhibitory effect of elevated glucose is mediated by an ATP-independent K + channel. The results also show that PIP 2 can determine the excitability of glucose-excited neurons.

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d-Glucose anomers in the nucleus of the vagus nerve can depress gastric motility of rats

Cited by 11 publications

References 10 publications

Gastric relaxation induced by hyperglycemia is mediated by vagal afferent pathways in the rat

Gastric relaxation induced by hyperglycemia is mediated by vagal afferent pathways in the rat

Glucose effects on gastric motility and tone evoked from the rat dorsal vagal complex

Electrophysiological identification of glucose-sensing neurons in rat nodose ganglia

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