Acute Stress Halts Hunger-Driven Food Seeking, Reversible by Anxiolytics and Ghrelin Agonists

Stress profoundly impacts eating behaviors, often leading to either overeating or appetite suppression. While chronic stress is frequently linked to comfort eating, the immediate effects of acute stress on hunger-driven food seeking are less understood. The paraventricular nucleus (PVN) of the hypothalamus is a crucial brain region involved in both stress responses and appetite regulation. This study aimed to elucidate the neural mechanisms by which acute stress suppresses hunger-driven food seeking and explore potential pharmacological interventions.

The study revealed that acute stress robustly suppressed hunger-driven food seeking in the animal model. This suppression was directly correlated with increased activation of neurons within the PVN, suggesting a critical role for this brain region in mediating the stress response on appetite. The most significant finding was the complete reversal of stress-induced food seeking suppression by both an anxiolytic drug and a ghrelin receptor agonist, indicating potential therapeutic targets. Specifically, the anxiolytic drug effectively mitigated the stress response, allowing hungry animals to resume normal food-seeking behaviors. Similarly, activation of ghrelin receptors, which typically promote hunger, successfully counteracted the stress-induced anorexia. Interestingly, refeeding after stress exposure also exhibited anxiolytic-like effects, suggesting a bidirectional relationship between stress, hunger, and emotional state. While specific quantitative data such as percentage reductions or p-values were not provided in the abstract, the findings strongly indicate a significant and measurable impact of both stress and the interventions.