Binge-like eating in early adolescence induces glial changes and dopaminergic dysregulation linked to risk-taking behaviors in rats.

Abstract

Intermittent access to palatable food is a risk factor for binge eating (BE) behavior development, characterized by rapid consumption of large amounts of food and a perceived loss of control. BE disorder usually emerges during adolescence and often co-occurs with neuropsychological alterations, including anxiety and impulsivity. These psychiatric conditions are associated with glial reactivity and dopaminergic dysfunction, yet the impact of adolescent BE on inflammatory markers in dopamine-targeted brain regions, as the nucleus accumbens (NAc) shell and prelimbic region of the medial prefrontal cortex (mPFC), and its relationship with risk-taking behaviors, remain largely unexplored. We exposed prepubertal male rats to four cycles of BE episodes by providing intermittent access to palatable food; anxiety-like and risk-taking/impulsive-like behaviors were assessed weekly over five weeks using the elevated-plus maze. By the third BE cycle, rats exhibited established binge-like eating behavior, reduced anxiety and heightened risk-taking/impulsive-like behaviors. These changes were associated with microglial reactivity, reduced astrocytic number, and reactive astrocytes in NAc and mPFC. BE rats also showed impaired dopaminergic signaling, reflected by low dopamine receptor type 2 density in both regions. Changes in dopamine and metabolite levels were indicative of enhanced dopamine release in NAc and decreased in the mPFC. Together, these findings show that adolescent binge-like eating induces glial reactivity and dopaminergic disturbances in key reward- and control-related brain regions, alongside changes in anxiety-like and risk-taking/impulsive-like behaviors. Such alterations during a critical developmental period may heighten vulnerability to psychiatric disorders characterized by impaired inhibitory control, including substance use disorders and attention-deficit/hyperactivity disorder.