The brain region responsible for cataplexy in orexin knockout mice, an animal model of narcolepsy 5, has already been reported to be the medial prefrontal cortex 6. We used the cataplexy that occurs in animal models of narcolepsy as an alternate quantitative animal model for happiness because cataplexy is triggered during behaviors associated with positive feelings, such as laughter in humans 3 and palatable foods in mice 4. If multiple reliable animal models for enjoyment or happiness are developed, a more solid idea of the neuronal mechanisms involved can be elucidated.

However, measuring only tongue protrusions is insufficient for evaluating possible happiness experienced from sources other than food. One exception are the reports from the Berridge group that used facial expressions such as tongue protrusions for an animal model of happiness and “liking” 2. In experimental animals, only limited reports are available presumably due to a shortage of reliable and quantitative measures of behaviors associated with happiness. However, more detailed information on the neurotransmitters and neuronal pathways involved in the interaction between emotion and bodily health is currently unavailable. Brain imaging studies in humans 1 predicted the possible involvement of several brain structures in happiness, such as the nucleus accumbens (NAc), the ventral pallidum, and the anterior cingulate cortex. Although its benefits are well known, the underlying brain mechanisms are not well understood. Happiness is a key emotion for both mental and physical well-being. Since the NAc is also implicated in motivated behavior, we propose that the NAc is one of the key brain structures involved in happiness and is a driving force for positive emotion-related behaviors.

These results demonstrated that the rostral part of the NAc plays a crucial role in triggering cataplexy and hedonic orofacial movements. Hedonic response in the DREADD experiment varied and showed both increases and decreases across mice.

As expected, the number of cataplexy bouts increased with activation and decreased with inactivation, and saline control injections showed no changes. Next, we used clozapine N-oxide to either activate or inactivate the NAc through viral DREADD expression. We also examined the hedonic response to palatable food by measuring the number of tongue protrusions in response to presentation of honey, which was also found to be negatively correlated to the lesion size. The number of cataplexy bouts was negatively correlated to the lesion size. We made a local lesion in the NAc using ibotenic acid and observed the animals’ behavior. Here we report that the rostral part of the nucleus accumbens (NAc) shell is strongly activated during the beginning of chocolate-induced cataplexy in orexin neuron-ablated mice. To further understand the brain mechanisms involved, we utilized the cataplexy that occurs in narcoleptic animal models as a quantitative behavioral measure because it is triggered by actions associated with happiness, such as laughter in humans and palatable foods in mice. Happiness is key for both mental and physical well-being.

Examples of cataplexy