AgRP neurons in the hypothalamic arcuate nucleus (ARC) regulate energy homeostasis and feeding behavior. This study used DREADD technology to specifically and reversibly activate AgRP neurons in mice, demonstrating that acute activation rapidly induces feeding, reduces energy expenditure, and increases fat stores. These effects reversed upon stimulation cessation. In contrast, inhibiting AgRP neurons in hungry mice reduced food intake, showing that AgRP neurons are both necessary and sufficient for feeding. Activation of AgRP neurons also increased motivation for feeding and food-seeking behavior, indicating their role in multiple levels of feeding behavior. DREADD technology is ideal for studying neural circuits regulating energy balance due to its ease of use and suitability for both acute and chronic regulation. The study used Cre-dependent AAV to target hM3Dq to AgRP neurons, allowing specific activation by CNO. CNO-induced depolarization of AgRP neurons increased firing rate and food intake, with effects lasting up to 8 hours. Chronic CNO injections caused significant weight gain, with weight loss upon drug withdrawal. Inhibiting AgRP neurons with hM4Di reduced food intake, showing their role in feeding behavior. AgRP neurons also drive intense motivated behavior for food, as shown by increased break points in a progressive ratio operant conditioning paradigm. Stimulation of AgRP neurons in food-deprived mice increased physical activity, indicating food-seeking behavior. These findings highlight the critical role of AgRP neurons in regulating feeding behavior and energy balance. The study provides a powerful tool for investigating the neural circuits underlying energy homeostasis.AgRP neurons in the hypothalamic arcuate nucleus (ARC) regulate energy homeostasis and feeding behavior. This study used DREADD technology to specifically and reversibly activate AgRP neurons in mice, demonstrating that acute activation rapidly induces feeding, reduces energy expenditure, and increases fat stores. These effects reversed upon stimulation cessation. In contrast, inhibiting AgRP neurons in hungry mice reduced food intake, showing that AgRP neurons are both necessary and sufficient for feeding. Activation of AgRP neurons also increased motivation for feeding and food-seeking behavior, indicating their role in multiple levels of feeding behavior. DREADD technology is ideal for studying neural circuits regulating energy balance due to its ease of use and suitability for both acute and chronic regulation. The study used Cre-dependent AAV to target hM3Dq to AgRP neurons, allowing specific activation by CNO. CNO-induced depolarization of AgRP neurons increased firing rate and food intake, with effects lasting up to 8 hours. Chronic CNO injections caused significant weight gain, with weight loss upon drug withdrawal. Inhibiting AgRP neurons with hM4Di reduced food intake, showing their role in feeding behavior. AgRP neurons also drive intense motivated behavior for food, as shown by increased break points in a progressive ratio operant conditioning paradigm. Stimulation of AgRP neurons in food-deprived mice increased physical activity, indicating food-seeking behavior. These findings highlight the critical role of AgRP neurons in regulating feeding behavior and energy balance. The study provides a powerful tool for investigating the neural circuits underlying energy homeostasis.