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The Fat Mass and Obesity-Associated Protein (FTO) Regulates Locomotor Responses to Novelty via D2R Medium Spiny Neurons

Journal article
Authors J. Ruud
J. Alber
A. Tokarska
L. E. Ruud
H. Nolte
N. Biglari
R. Lippert
A. Lautenschlager
P. E. Ciealak
L. Szumiec
M. E. Hess
H. S. Bronneke
M. Kruger
Hans Nissbrandt
T. Korotkova
G. Silberberg
J. R. Parkitna
J. C. Bruning
Published in Cell Reports
Volume 27
Issue 11
Pages 3182-3189.e9
ISSN 2211-1247
Publication year 2019
Published at Institute of Neuroscience and Physiology, Department of Pharmacology
Pages 3182-3189.e9
Language en
Keywords gene-expression, neural mechanisms, mice, rna, variant, interneurons, methylation, impulsivity, identification, enrichment, Cell Biology, ates of america, v104, p1325, rfen cr, 1990, science, v250, p1429, hiffmann sn, 1993, journal of neuroscience, v13, p1080
Subject categories Endocrinology and Diabetes


Variations in the human FTO gene have been linked to obesity and altered connectivity of the dopaminergic neurocircuitry. Here, we report that fat mass and obesity-associated protein (FTO) in dopamine D2 receptor-expressing medium spiny neurons (D2 MSNs) of mice regulate the excitability of these cells and control their striatopallidal globus pallidus external (GPe) projections. Lack of FTO in D2 MSNs translates into increased locomotor activity to novelty, associated with altered timing behavior, without impairing the ability to control actions or affecting reward-driven and conditioned behavior. Pharmacological manipulations of dopamine D1 receptor (D1R)- or D2R-dependent pathways in these animals reveal altered responses to D1- and D2-MSN-mediated control of motor output. These findings reveal a critical role for FTO to control D2 MSN excitability, their projections to the GPe, and behavioral responses to novelty.

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