| First Author | Wang L | Year | 2008 |
| Journal | Neuroreport | Volume | 19 |
| Issue | 8 | Pages | 873-6 |
| PubMed ID | 18463504 | Mgi Jnum | J:136697 |
| Mgi Id | MGI:3796796 | Doi | 10.1097/WNR.0b013e3282ffda5e |
| Citation | Wang L, et al. (2008) Abnormal colonic motility in mice overexpressing human wild-type alpha-synuclein. Neuroreport 19(8):873-6 |
| abstractText | The presynaptic protein alpha-synuclein (alphaSyn) has been implicated in both familial and sporadic forms of Parkinson's disease. We examined whether human alphaSyn-overexpressing mice under Thy1 promoter (Thy1-alphaSyn) display alterations of colonic function. Basal fecal output was decreased in Thy1-alphaSyn mice fed ad libitum. Fasted/refed Thy1-alphaSyn mice had a slower distal colonic transit than the wild-type mice, as monitored by 2.2-fold increase in time to expel an intracolonic bead and 2.9-fold higher colonic fecal content. By contrast, Thy1-alphaSyn mice had an increased fecal response to novelty stress and corticotropin releasing factor injected intraperipherally. These results indicate that Thy1-alphaSyn mice display altered basal and stress-stimulated propulsive colonic motility and will be a useful model to study gut dysfunction associated with Parkinson's disease. |
