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Nuclear receptor Nr4a1 regulates striatal striosome development and dopamine D1 receptor signaling

  • Maria Daniela Cirnaru
    ,
  • Chiara Melis
    ,
  • Tomas Fanutza
    ,
  • Swati Naphade
    ,
  • Kizito Tshitoko Tshilenge
    ,
*Corresponding author for this work
  • Icahn School of Medicine at Mount Sinai
    ,
  • Buck Institute for Age Research
    ,
  • University of Florida
    ,
  • Stony Brook University
Scholary Output:
Contribution to journal
Article
Peer-review

Open access

Abstract

The GABAergic medium-size spiny neuron (MSN), the striatal output neuron, may be classified into striosome, also known as patch, and matrix, based on neurochemical differences between the two compartments. At this time, little is known regarding the regulation of the development of the two compartments. Nr4a1, primarily described as a nuclear receptor/immediate early gene involved in the homeostasis of the dopaminergic system, is a striosomal marker. Using Nr4a1-overexpressing and Nr4a1-null mice, we sought to determine whether Nr4a1 is necessary and/or sufficient for striosome development. We report that in vivo and in vitro, Nr4a1 and Oprm1 mRNA levels are correlated. In the absence of Nr4a, there is a decrease in the percentage of striatal surface area occupied by striosomes. Alterations in Nr4a1 expression leads to dysregulation of multiple mRNAs of members of the dopamine receptor D1 signal transduction system. Constitutive overexpression of Nr4a1 decreases both the induction of phosphorylation of ERK after a single cocaine exposure and locomotor sensitization following chronic cocaine exposure. Nr4a1 overexpression increases MSN excitability but reduces MSN long-term potentiation. In the resting state, type 5 adenylyl cyclase (AC5) activity is normal, but the ability of AC5 to be activated by Drd1 G-protein-coupled receptor inputs is decreased. Our results support a role for Nr4a1 in determination of striatal patch/matrix structure and in regulation of dopaminoceptive neuronal function.

Publication Information

Output type

Scholary Output:
Contribution to journal
Article
Peer-review

Original language

English (US)

Article number

ENEURO.0305-19.2019

Journal (Volume, Issue Number)

eNeuro (Volume 6, Issue 5)

Publication milestones

  • Published - 2019

Publication status

Published - 2019

Publication IDs

  • Scopus: 85073123910
  • PubMed: 31541002

Publication metrics

Metrics

SciVal
citations
6
Fractional count
1
Fractional count
0.10
Fractional count
9
Fractional count
0.90
Fractional count
1
Fractional count
1
SciVal
FWCI
0.91
SciVal
Author count
10
SciVal
Paper percentile
80
Scopus
citations

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Captures
29
Citation count
18

Funding Details

Received August 2, 2019; accepted August 29, 2019; First published September 20, 2019. The authors declare no competing financial interests. Author contributions: M.-D.C., C.M., T.F., S.N., K.A.M., J.L.P., L.M.E., and M.E.E. designed research; M.-D.C., C.M., T.F., S.N., K.-T.T., and B.S.M. performed research; M.-D.C., C.M., T.F., S.N., K.-T.T., B.S.M., K.A.M., and J.L.P. analyzed data; M.-D.C., B.S.M., K.A.M., J.L.P., L.M.E., and M.E.E. wrote the paper. This research was supported by the Collaborative Center for X-linked Dystonia Parkinsonism; and by Department of Health and Human Services | National Institutes of Health | National Institute of Neurological Disorders and Stroke Grant R01-NS-100529 (to L.M.E. and M.E.E.). *M.D.C. and C.M. contributed equally to this work. Correspondence should be addressed to Michelle E. Ehrlich at [email protected]. https://doi.org/10.1523/ENEURO.0305-19.2019 Copyright © 2019 Cirnaru et al. This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license, which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.
FundersFunding numbers
FNIH
R01-NS-100529
NIDA
K02DA026405