Exercise training rescues the electrical activity of liver-projecting DMNV neurones in response to oxytocin in spontaneously hypertensive rats.

A neural circuit between the paraventricular nucleus of the hypothalamus (PVN) and the dorsal motor nucleus of the vagus (DMNV) constitutes part of an important parasympathetic autonomic pathway that controls hepatic glucose production. Intracerebroventricular injection of insulin activates oxytocinergic neurones in the PVN and elicits the release of oxytocin into the circulation, which plays an important role in the metabolism of glucose. Moreover, the central action of insulin can reduce the concentration of glucose in blood taken from the hepatic vein of Wistar rats via activation of vagal efferent nerves to the liver. This mechanism is impaired in sedentary spontaneously hypertensive rats (SHR). Because aerobic exercise increases vagal tone, partly mediated by increasing the oxytocinergic connections between the PVN and DMNV, we hypothesised that oxytocin (OT) might alter the excitability of liver-projecting DMNV neurones. Thus, we investigated the effects of OT on electrical properties of the liver-projecting DMNV neurones from Wistar, SHR subjected to 4 weeks of exercise training, as well sedentary controls, using whole cell patch-clamping. The results show that OT increased the resting membrane potential of DMNV neurones in Wistar rats, as well as the firing frequency of these cells, but not in sedentary SHR. However, in SHR subjected to 4 weeks of exercise training, the effects of OT on liver-projecting DMNV neurones of were similar to those seen in Wistar rats. These findings show that OT elicits similar changes in the electrophysiological properties of liver-projecting DMNV neurones of Wistar and exercise-trained but not sedentary SHR. These results indicate that exercise training can restore the sensitivity of liver-projecting DMNV neurones of exercise-trained SHR to OT.