Caffeine Modulates Food Intake Depending on the Context That Gives Access to Food: Comparison With Dopamine Depletion

Abstract

Caffeine is a methylxanthine consumed in different context s to potentiate alertness and reduce fatigue. However, caffeine can induce anxiety at hig h doses. Caffeine is also a minor psychostimulant that seems to act as an appetite supp ressant, but there are also reports indicating that it could stimulate appetite. D opamine also is involved in food motivation and in behavioral activation. In the present ser ies of experiments, we evaluated the effects of acute administration of caffeine on food cons umption under different access conditions. CD1 male adult mice had access to highly palatab le food (50% sucrose) in a restricted but habitual context, under continuous or in termittent access as well as under anxiogenic, or effortful conditions. Caffeine (2.5– 20.0 mg/kg) increased intake at the highest dose under familiar continuous and intermitten t access. However, this high dose reduced food intake in the dark-light paradigm. In cont rast, a dopamine-depleting agent, tetrabenazine (TBZ; 1.0–8.0 mg/kg) did not affect fo od intake in any of those experimental conditions. In the T-maze-barrier task that e valuates seeking and taking of food under effortful conditions, caffeine (10.0 mg/kg) d ecreased latency to reach the food, but did not affect selection of the high-food density a rm that required more effort, or the total amount of food consumed. In contrast, TBZ (4.0 mg /kg) reduced selection of the high food density arm with the barrier, thus affecting amount of food consumed. Interestingly, a small dose of caffeine (5.0 mg/kg) was able to reverse the anergia-inducing effects produced by TBZ in the T-maze. These results suggest that caffeine can potentiate or suppress food consumption depending on the context. More over, caffeine did not change appetite, and did not impair orientation toward food under effortful conditions, but it rather helped to achieve the goal by improving speed an d by reversing performance to normal levels when fatigue was induced by dopamine deplet ion.