@article{faf5ffaa882a46b5b34aaf64852d6d15,
title = "Defining dysbiosis in disorders of movement and motivation",
abstract = "The gut microbiota has emerged as a critical player in shaping and modulating brain function and has been shown to influence numerous behaviors, including anxiety and depression-like behaviors, sociability, and cognition. However, the effects of the gut microbiota on specific disorders associated with thalamo-cortico-basal ganglia circuits, ranging from compulsive behavior and addiction to altered sensation and motor output, are only recently being explored. Wholesale depletion and alteration of gut microbial communities in rodent models of disorders, such as Parkinson{\textquoteright}s disease, autism, and addiction, robustly affect movement and motivated behavior. A new frontier therefore lies in identifying specific microbial alterations that affect these behaviors and understanding the underlying mechanisms of action. Comparing alterations in gut microbiota across multiple basal-ganglia associated disease states allows for identification of common mechanistic pathways that may interact with distinct environmental and genetic risk factors to produce disease-specific outcomes.",
keywords = "Addiction, Basal ganglia, Compulsive behavior, Gut microbiota, Motor function, Parkinson{\textquoteright}s",
author = "Fields, {Christopher T.} and Sampson, {Timothy R.} and Bruce-Keller, {Annadora J.} and Kiraly, {Drew D.} and Hsiao, {Elaine Y.} and {de Vries}, {Geert J.}",
note = "Funding Information: This work was supported by National Institute of Health Grants MH112369 to C.T.F., MH110117 to A.J.B.-K., DA044308 to D.D.K., OD017924 to E.Y.H., and MH108345 to G.J.d.V.; the Brain and Behavior Research Foundation to D.D.K.; the Larry L. Hillblom Foundation to T.R.S.; and the Office of Naval Research, Multidisciplinary University Research Initiative to E.Y.H. Funding Information: Received Sept. 5, 2018; revised Sept. 28, 2018; accepted Sept. 28, 2018. This work was supported by National Institute of Health Grants MH112369 to C.T.F., MH110117 to A.J.B.-K., DA044308toD.D.K.,OD017924toE.Y.H.,andMH108345toG.J.d.V.;theBrainandBehaviorResearchFoundationto D.D.K.; the Larry L. Hillblom Foundation to T.R.S.; and the Office of Naval Research, Multidisciplinary University Research Initiative to E.Y.H. The authors declare no competing financial interests. Correspondence should be addressed to Dr. Christopher T. Fields, Neuroscience Institute, Georgia State University, Atlanta, GA 30303. E-mail: cfields18@student.gsu.edu. T.R.Sampson{\textquoteright}spresentaddress:DepartmentofPhysiology,EmoryUniversitySchoolofMedicine,EmoryUniver-sity, Atlanta, GA 30329. DOI:10.1523/JNEUROSCI.1672-18.2018 Copyright {\textcopyright} 2018 the authors 0270-6474/18/389414-09$15.00/0 Publisher Copyright: {\textcopyright} 2018 the authors.",
year = "2018",
month = oct,
day = "31",
doi = "10.1523/JNEUROSCI.1672-18.2018",
language = "English",
volume = "38",
pages = "9414--9422",
journal = "Journal of Neuroscience",
issn = "0270-6474",
publisher = "Society for Neuroscience",
number = "44",
}