Topic: Activity-Based Anorexia

Anorexia nervosa (AN) is a serious eating disorder prevalently widespread in female subjects, characterized by a severe restriction of caloric intake, fear of becoming fat, dysmorphophobia and hyperactivity (DSM–5). Nowadays growing evidence shed light about the involvement of immunoinflammatory pathways in AN, considering the rise in the peripheral levels of pro-inflammatory cytokines in patients (Solmi et al., 2015). Furthermore, neuroinflammation may be an additional characteristic of AN (Rahimian et al., 2021), since it has been observed in other psychiatric disorders. The Activity-Based A

Hyperactivity is a persistent symptom of anorexia nervosa (AN) that often precedes occurrence of the disease, and constitutes a major barrier to recovery. Alteration of mesolimbic dopamine transmission has been hypothesized as a critical factor for the development and maintenance of AN and hyperactivity. However, the nature of dopamine dysfunction in AN, and the underlying mechanisms remain unclear. We therefore aimed at i) characterizing the impact of the activity-based anorexia (ABA) model on ventral tegmental area dopamine (VTADA) neurons and ii) determining whether restoring activity of VT

A reduction of food intake – and concurrent loss of body weight – in combination with physical hyperactivity are main symptoms of the eating disorder anorexia nervosa. Continuous loss of fat mass results in hypoleptinemia, which initiates multiple starvation-related adaptive functions. Although leptin administration showed beneficial effects in treatment of symptoms of anorexia nervosa, including anxiety, neuronal mechanisms of possible anxiety-relieving action of leptin are not known.Here, combining calcium imaging and opto- or chemogenetics in freely behaving mice, we investigated functions