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GLP-1R gene delivery to the dLS of GLP-1R deficient mice resulted in reduced cocaine-induced CPP and locomotor activity without changing anxiety behaviors (Harasta et al., Amphetamine Ex-4 (2.4 g/kg) decreased amphetamine-induced hyperlocomotion, CPP, and accumbal dopamine release without affecting spontaneous locomotor activity and accumbal dopamine release in normal conditions (Egecioglu et al., 2005)

is supported by the European Union NextGenerationEU (PNRRPOC202312377319), the Next Gen Clinician Scientist 2024 of the AIRC (project 30203), the Fondo Italiano per la Scienza (FIS00001711), the European Research Council (ERC-StG MicroRestore-101221279), the Joint Programming Initiative on Antimicrobial Resistance (DONATE ERP-2022-23682517) and the SEERAVE Foundation

Research has characterised Semaglutides beta cell incretin biology in primary human and rodent islets and beta cell line models examining sustained cAMP accumulation kinetics under long-acting GLP-1R stimulation, insulin secretion dose-response relationships across glucose concentration ranges establishing glucose-dependency of Semaglutide-driven incretin potentiation, first and second phase insulin secretory responses under chronic GLP-1R occupancy, and the beta cell adaptation responses to sustained versus episodic GLP-1R stimulation