Adaptive gene regulation in the Striatum of RGS9-deficient mice.

ABSTRACT:

Background

RGS9-deficient mice show drug-induced dyskinesia but normal locomotor activity under unchallenged conditions.

Results

Genes related to Ca2+ signaling and their functions were regulated in RGS9-deficient mice.

Conclusion

Changes in Ca2+ signaling that compensate for RGS9 loss-of-function can explain the normal locomotor activity in RGS9-deficient mice under unchallenged conditions.

Significance

Identified signaling components may represent novel targets in antidyskinetic therapy. The long splice variant of the regulator of G-protein signaling 9 (RGS9-2) is enriched in striatal medium spiny neurons and dampens dopamine D2 receptor signaling. Lack of RGS9-2 can promote while its overexpression prevents drug-induced dyskinesia. Other animal models of dru

SUBMITTER: Busse K 

PROVIDER: S-EPMC3963927 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature