A Neurocomputational Model for the Relation Between Hunger, Dopamine and Action Rate

Abstract

A number of conditioning experiments utilize food as a reward. Hunger is considered to be a critical factor governing the animal's behavior in these experiments. Despite its significance, most theories of animal conditioning fail to take hunger into consideration while analyzing the behavioral data. In this paper, we analyze the neuroscientific data supporting the hypothesis that hunger and food consumption affect the brain's dopamine system, which in turn governs the animal's behavior. According to this hypothesis, chronic hunger results in a decrease in the extra-cellular dopamine levels in the animal's brain. This decrease is believed to trigger a series of reactions that increase the responsivity of the phasic dopamine system. A direct consequence of this is an increased vigor of all dopamine-dependent behaviors. The level of extra-cellular dopamine is also modulated by the process of food consumption via the neurotransmitter Acetylcholine. Food consumption raises the dopamine above the baseline level. This rise depends on the animals' hunger, which when satisfied increases the level of Acetylcholine, which causes the dopamine level to fall back to the baseline. Thus, extra-cellular dopamine governs the response vigor, with an increase in dopamine resulting in a more vigorous response. This paper makes two primary contributions. Firstly, we present an abstract mathematical model based on the above hypothesis. Our mathematical model is able to provide a simple explanation for a number of behavioral findings. Another contribution of this paper is the development of a neurocomputational Leabra model of dopamine and acetylcholine activity in the basal ganglia to incorporate hunger and satiation. The experimental results obtained from this neural model are also largely in agreement with behavioral findings.