Synaptic and Intrinsic Plasticity Mediated by CCK-type Signaling Coordinates Behavioral Changes During Motivational State Shifts
Transitions from hunger to satiety involve multiple behavioral changes, including modulation and inhibition of feeding behavior. Cholecystokinin (CCK), a key satiety peptide in mammals, plays a critical role in these processes, though whether and how CCK might induce satiety via synaptic and intrinsic plasticity remain unclear. Here, we demonstrate that CCK acts as a classical brain-gut peptide in a protostome, mollusk Aplysia. CCK neurons, located in the gut, project centrally to release CCK at the site of the feeding pattern generator. In vivo, CCK reduced food intake, while in vitro, it shifted motor patterns towards egestion and inhibited feeding programs. Mechanistically, CCK primarily modulated the excitability of the egestive-promoting B20 interneuron and suppressed synaptic inputs to protraction motoneurons, thereby altering program type and inhibiting feeding program generation. These findings highlight the importance of both synaptic and intrinsic plasticity in specific circuit elements for implementing motivational shifts induced by satiety peptides. Overall design: Smart single-cell sequencing of Aplysia B20 neuron and B34 neuron