Tu1973 Gut Microbiota Regulate Murine Gastrointestinal Motility Through a Toll-Like Receptor 4 Dependent Pathway

Abstract

G A A b st ra ct s reduction of fecal pellets also occurred in the first 15 min of novel environment. Thy1-aSyn mice (8-10 months) displayed increased α-synuclein in myenteric plexi with abundant varicose terminals surrounding pChAT-immunoreactive (ir) neurons and only a few, nNOSir neurons. There were no conspicuous changes in pChATand nNOS-ir neurons, and THand VIP-ir nerve fibers, or proteinase K-resistant α-synuclein aggregates at the ages examined. GE was not altered in Thy1-aSyn mice aged 4 to 18 months. Conclusions: The occurrence of colonic dysfunction in Thy1-aSyn mice several months before the loss of striatal dopamine together with the histological data support the hypothesis that over-production of presynaptic α-synuclein in colonic myenteric ganglia could interfere with cholinergic neuronal activation, causing early functional bowel symptoms in PD. Supported by Michael J. Fox Foundation (Target validation grant), the Morris K. Udall Parkinson's Disease Research Center of Excellence at UCLA (P50NS38367), center grant NIHDDK 41301 (Animal Core), RO1 DK 57238; center grant P50 DK064539 for Oppenheimer Family Center for Neurobiology of Stress and VA Career Scientist Award