Paraventricular nucleus anandamide signaling alters eating and substrate oxidation.

In the central nervous system, the endocannabinoid anandamide [N-arachidonoylethanolamine (AEA)] is believed to increase food intake through on-demand activation of hypothalamic circuits. The present study examined the effects of hypothalamic paraventricular nucleus (PVN) injections of AEA (25-400 pmol) on food intake and energy substrate oxidation [respiratory quotient (RQ)]. PVN administration of AEA increased eating behavior and RQ, indicating enhanced carbohydrate oxidation.

6-Hydroxydopamine lesions of the ventral tegmental area suppress ghrelin's ability to elicit food-reinforced behavior.

While past research suggests that ghrelin stimulates appetite through an action on hypothalamic signaling, recent evidence indicates that the peptide acts via mesotelencephalic dopamine neurons to alter appetitive motivation. In the present study, rats were trained to operantly respond for food on a progressive ratio PR5 schedule until stable breakpoints were established. Ghrelin (30-300 pmol) was then injected directly into the ventral tegmental area (VTA) and the 300 pmol dose was observed to increase breakpoint.