Paraventricular nucleus-microinjected glucose increases food intake in 18 h food-deprived rats: A central regulatory mechanism on serum ghrelin and leptin levels.

Our previous study demonstrated that glucose acts in hypothalamic paraventricular nucleus (PVN) to increase gastric acid secretion. However, there is no evidence to show the role of the hypothalamic PVN-microinjected glucose on food intake. On the other hand, it is known that ghrelin and leptin play important roles in food intake. The current study investigated the association between PVN-microinjected glucose and food intake and plasma ghrelin-leptin levels. After the PVN microinjection of glucose, food intake was measured. In other groups, ELIZA kits were used to obtain ghrelin, leptin, insulin and glucose concentrations. All experiments were done in18 h food-deprived rats. The findings revealed that the PVN-microinjected glucose increased food intake in a dose-dependent manner. The stimulatory effect of glucose persisted for more than 2 h. Interestingly, it was found that PVN microinjection of glucose stimulates plasma ghrelin and decreases plasma leptin levels without any effect on plasma insulin and glucose concentrations over 1 h. The results of the present study suggest that the PVN glucose-mediated cells may be involved in the regulatory mechanisms of food intake. This stimulatory effect seems to be mediated, at least in part, through central nervous system regulatory mechanisms of plasma leptin and ghrelin levels.

Role of orexin receptors within the dentate gyrus of the hippocampus in antinociception induced by chemical stimulation of the lateral hypothalamus in the tail-flick test as a model of acute pain in rats.

The dentate gyrus (DG) as a part of the hippocampal formation is considered one of the brain areas involved in pain perception. The orexin neurons in the lateral hypothalamus (LH) also show connections to regions engaged in the circuitry of pain modulation and many studies have shown their potential to alter pain transmission through the nervous system. However, the role of orexin receptors (OXRs) of the DG in mediation of antinociceptive responses induced by the LH stimulation in rats has not yet been investigated. Hence, the present study was an attempt to examine the role of OXRs located within the DG in the pain modulation induced by chemical stimulation of the LH. Adult male Wistar rats weighing 220-250 g were unilaterally implanted with two separate cannulae into the LH and DG. Intra-DG administration of the orexin-1 receptor (OX1R) antagonist, SB334867 or the orexin-2 receptor (OX2R) antagonist, TCS OX2 29 was performed just 5 min before intra-LH carbachol microinjection. Antinociceptive effects were measured using the tail-flick apparatus. The results showed that OX1R and OX2R antagonists dose-dependently decreased the antinociceptive effect of carbachol. In addition, the effective dose of SB334867 was lesser than that of TCS OX2 29, which indicates the more prominent role of OX1R of the DG in carbachol-induced antinociception. None of the antagonists had any significant effect when administrated without intra-LH carbachol microinjection. It seems to be a neural circuit includes the LH and DG, which plays a major role in the neural basis of pain modulation.