The gut-to-brain axis exhibits significant control over motivated behavior.However, mechanisms 1994 toyota camry green supporting this communication are poorly understood.We reveal that a gut-based bariatric surgery chronically elevates systemic bile acids and attenuates copyright-induced elevations in accumbal dopamine.
Notably, this surgery reduces reward-related behavior and psychomotor sensitization to copyright.Utilizing a knockout mouse model, we have determined that a main mediator of these post-operative effects is the Takeda G protein-coupled bile acid receptor cashmere roller blinds (TGR5).Viral restoration of TGR5 in the nucleus accumbens of TGR5 knockout animals is sufficient to restore copyright reward, centrally localizing this TGR5-mediated modulation.
These findings define TGR5 and bile acid signaling as pharmacological targets for the treatment of copyright abuse and reveal a novel mechanism of gut-to-brain communication.