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Available4.9
30 reviewsSUMMARYTransitions from hunger to satiety involve multiple behavioral changes, including modulation and inhibition offeeding behavior. In mammals, cholecystokinin (CCK) is a key satiety peptide implicated in these processes;however, whether and how CCK might induce satiety via synaptic and intrinsic plasticity remains unclear.Here, we investigate CCK-type signaling in the protostome mollusk Aplysia californica. We demonstratethat Aplysia CCK (apCCK) acts as a conserved brain-gut peptide. Gut-localized apCCK-expressing neuronsproject centrally and release apCCK near the feeding-pattern generator. In vivo, apCCK suppresses foodintake, while in vitro, it shifts motor output toward egestive patterns and inhibits feeding programs. Mechanistically, apCCK modulates the excitability of the egestive-promoting B20 interneuron and suppresses synaptic input to protraction-phase motoneurons, thereby altering program selection and inhibiting feeding-program generation. These findings highlight the importance of both synaptic and intrinsic plasticity in specificcircuit elements for implementing motivational shifts driven by satiety signaling.
4.9
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4.5
13 reviews