Regulation of PVT‐CeA Circuit in Deoxynivalenol‐Induced Anorexia and Aversive‐Like Emotions

Abstract Neuronal plasticity in the central amygdala (CeA) is essential for modulating feeding behaviors and emotional responses, potentially influencing reactions to Deoxynivalenol (DON). Acute oral administration of DON elicits a dose‐responsive reduction in food intake, accompanied by pronounced alterations in locomotor activity and feeding frequency. This study investigates circuitry adaptations that mediate DON's effects on feeding, by targeting of GABA neurons in the CeA. Following exposure to DON, an increase in connectivity between the paraventricular nucleus of the thalamus (PVT) and CeA GABA neurons is observed, suggesting the involvement of this pathway in DON's adverse effects on feeding and emotional states. Chemogenetic and optogenetic manipulations of CeA GABA neurons resulted in substantial alterations in mice's feeding and overall activity. These findings suggest that CeA GABA neurons are involved in DON‐induced anorexia and aversive‐like emotional responses. Additionally, the administration of the SCN10A antagonist (A‐803467) effectively mitigated DON‐induced anorexia and aversive‐like emotions, highlighting the pivotal role of the PVT‐CeA circuit and CeA GABA neurons in regulating the physiological and emotional impacts of DON. These findings have significant implications for public health and clinical interventions, offering potential therapeutic strategies to mitigate DON's adverse effects on human health.