| First Author | Reddy IA | Year | 2018 |
| Journal | PLoS Biol | Volume | 16 |
| Issue | 7 | Pages | e2006682 |
| PubMed ID | 30048457 | Mgi Jnum | J:264088 |
| Mgi Id | MGI:6192791 | Doi | 10.1371/journal.pbio.2006682 |
| Citation | Reddy IA, et al. (2018) Bile diversion, a bariatric surgery, and bile acid signaling reduce central cocaine reward. PLoS Biol 16(7):e2006682 |
| abstractText | The gut-to-brain axis exhibits significant control over motivated behavior. However, mechanisms supporting this communication are poorly understood. We reveal that a gut-based bariatric surgery chronically elevates systemic bile acids and attenuates cocaine-induced elevations in accumbal dopamine. Notably, this surgery reduces reward-related behavior and psychomotor sensitization to cocaine. 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 (TGR5). Viral restoration of TGR5 in the nucleus accumbens of TGR5 knockout animals is sufficient to restore cocaine reward, centrally localizing this TGR5-mediated modulation. These findings define TGR5 and bile acid signaling as pharmacological targets for the treatment of cocaine abuse and reveal a novel mechanism of gut-to-brain communication. |
