The developmental increase in anorexigenic drive in early ontogenesis of rats is linked to changes in hypothalamic neuronal circuits. In contrast to adults, young postnatal rats show an underdeveloped anorexigenic system due to the immaturity of arcuate nucleus (ARC) projections. Patch-clamp recordings in hypothalamic slices revealed that neurosecretory parvocellular neurons in the paraventricular nucleus (PVN) undergo significant developmental changes in their responsiveness to anorexigenic and orexigenic peptides. While neuropeptide Y (NPY) remains functionally active from postnatal day (PD) 2, the sensitivity to α-melanocyte-stimulating hormone (α-MSH) emerges later. Immunostaining indicated a progressive increase in corticotropin-releasing hormone (CRH) expression, suggesting a key role in the maturation of anorexigenic circuits. The developmental increase in the number of α-MSH-sensitive GABAergic synapses and CRH-positive neurons may contribute to the regulatory mechanisms underlying appetite suppression in early ontogenesis. These findings also provide insights into the inefficiency of leptin signaling in neonatal life.