Search

The rates of oxygen consumption, colonic and interscapular brown adipose tissue temperature, and discharge of sympathetic nerves innervating the same tissue were recorded before and after orbital frontal cortex stimulation in three groups of rats. These groups consisted of animals with electrolytic lesions of the nucleus medialis septi, with lesions of nucleus lateralis septi or with sham lesions. The values of all the variables considered were similar during the pre-stimulation time in the three groups of rats. There was an increase in all the parameters in sham-lesioned animals after electrical stimulation, while no changes were found in the two groups of injured rats. The results showed that the frontal cortex is involved in the control of thermogenesis through the activation of the sympathetic nervous system. Medial and lateral septal nuclei, in spite of their neurochemical and pharmacological differences, share a common role in the pathway from the frontal cortex to the hypothalamic area and the amygdala, which in turn drive the sympathetic nervous system.

Aim: Hypocretin 1 is an hypothalamic neuropeptide that induces an increase in food intake when administered into the cerebral lateral ventricle. As it is well known that the medial hypothalamus (MH) is involved in the feeding behaviour also through GABAergic circuits, the aim of this experiment was to investigate the effect of an hypocretin 1 intracerebroventricular (icv) injection on the extracellular levels of GABA in the MH. Methods: GABA levels in the MH were evaluated in six rats by microdialysis and high performance liquid chromatography-electrochemical detection 30 min before and every 30 min for an over all period of 6 h after an icv injection of hypocretin 1. The same procedure was used in another group of six rats but saline was injected into the lateral ventricle as control. Results: The results show that extracellular GABA increases in the MH after the injection of hypocretin 1 at 60 min and at 3 h after the injection. Conclusion: This finding suggests a possible mechanism by which hypocretin 1 should induce hyperphagia in the first hour after injection. As it is already known that the inhibition of the MH by injection of GABA causes an increase of food intake, it is possible that hypocretin 1 causes an increase in food intake by increasing the GABA release in the MH. The lack of an increase in the GABA level after the fourth hour is consistent with the lack of an increase in food intake at this time, as we observed in previous experiments. The finding of a biphasic increase in the GABA level, at 60 min and at 3 h, was unexpected and should be further investigated.