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Additionally, chronic liraglutide treatment protected synaptic plasticity impairments and, in contrast to fluoxetine, attenuated the inhibition of long-term potentiation in the hippocampus, which was induced by corticosterone in 30-day treatment [49]

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Furthermore, in a more physiological setting, CCK-1R antagonism during a fasting-refeeding paradigm results in hyperglycemia, highlighting the glucoregulatory relevance of CCK-8 signaling 194