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

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). In the in vivo anaesthetized rat preparation, unilateral microinjection of d -glucose (10 or 50 m m (60 nl) −1 ) in mNTS produced inhibition of gastric motility and an increase in intragastric pressure. d -glucose had no effect in the DMV. 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 m m to 15 or 30 m m 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). 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. 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.