A genetically-defined population of amygdalofugal neurons promotes suckling and early postnatal growth
Suckling by newborns is an instinctive behavior defining the mammalian class. Yet, due to experimental difficulty in assessing neural function in the very young, little is known about the neural control of this fundamental behavior. Here we develop molecular-genetic approaches to interrogate neuronal connectivity and function in newborn mice and used these tools to identify a population of pro-dynorphin (PDYN) and somatostatin (SST) expressing neurons in the central amygdala that are activated during suckling. CeAPDYN+SST+ neurons connect with brainstem areas mediating oral sensorimotor and reward function in adults, and their ablation in newborns decreases suckling vigor and impairs growth. These results uncover the crucial role of a specific neuronal population of the central amygdala in maintaining the infants propensity to suckle and thrive throughout infancy.