Adrenalectomy abolishes the food-induced hypothalamic serotonin release in both normal and monosodium glutamate-obese rats.

Corticosteroids influence energy homeostasis through centrally-mediated stimulation of energy intake and inhibition of expenditure, while central serotonin (5-HT) has opposite effects. Both serotonergic dysfunction and high glucocorticoid levels may be relevant in obesity. The neurotoxin monosodium glutamate (MSG) induces a non-hyperphagic and hypometabolic obesity with hypercorticosteronemia. We investigated the influence of corticosterone levels on the serotonergic system of MSG-obese and control rats. Applying microdialysis, we found a similar feeding-induced stimulation of serotonin release in the lateral hypothalamus (LH) in sham-adrenalectomized control and MSG rats. The concomitant serum corticosterone variations were markedly distinct between them, in that an increase occurred in the control group, while the initially high levels of the MSG rats decreased with feeding. It is suggested that this lowering of corticosterone prevented a higher serotonergic activation, which would lead to a higher meal-induced thermogenesis and a better adequation of the caloric intake to a low metabolism. Adrenalectomy completely abolished the feeding-evoked serotonergic stimulation in both groups. This observation demonstrates that glucocorticoids are necessary for food intake to acutely stimulate 5-HT release and indicates that serotonergic activity in the LH is not likely to participate in the adrenalectomy-induced attenuation of the MSG-obesity.