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

Abstract

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...

Excitatory and inhibitory local circuit input to the rat dorsal motor nucleus of the vagus originating from the nucleus tractus solitarius

“…Electrical stimulation of the NTS resulted in eEPSCs and eIPSCs in the DMV in almost every instance, supporting and expanding upon previous findings [4,5,12,17,23]. However, due to abundant axons in the caudal NTS and DMV arising from neurons in other CNS regions, from other levels of the NTS, or from the solitary tract, it is impossible to know if electrically evoked PSCs in the DMV were the result of activity arising from neurons of the caudal NTS.…”

“…Although most have focused on an inhibitory connection, [11,18,25,32] the existence of an excitatory connection has also been suggested [5,32]. Anatomical evidence for the existence of a direct connection between the NTS and DMV is based primarily on dye injections into the NTS [23], retrograde transneuronal viral labeling of NTS neurons after infection of terminal fields in the viscera [6,12], ormorphological identification of neurons known to project to DMV [12]. However, these studies do not directly demonstrate synaptic connections between the nuclei and provide little information about the function or organization of connectivity with individual DMV cells.…”

Presynaptic NMDA receptor-mediated modulation of excitatory neurotransmission in the mouse dorsal motor nucleus of the vagus

“…GABA neurons are prominent in the medial NTS, which project inhibitory inputs to gastrointestinal-projecting regions of the DMV (Davis et al 2004;Derbenev et al 2004;Ferreira et al 2001;Glatzer et al 2007;Travagli et al 1991). Inhibitory input to DMV cells has been found to be modulated through a variety of preterminal receptors, including those for monoamines, catecholamines, peptides, and lipids, in addition to glutamate receptors on GABA terminals (Browning and Travagli 2007;Derbenev et al 2006;Glatzer et al 2007;Travagli and Gillis 1995;Zsombok et al 2011).…”

Effect of anesthetics on gastric damage using two models of portal hypertension

“…Moreover, it has been proposed that glucose acts in the hepatic portal area to inhibit hepatic afferent nerve traffic to the brain which results in a reflex reduction in efferent activity of the gastric vagus nerve [26,28] . It has also been proposed that glucose acts in the brain to alter control of vagal mediated gastric motility [25,27,29,30] . Xylazine is analogue of clonidine and its effect as a α2-adrenergic agonist is known.…”