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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Mouse Gpr88

ABSTRACT: Gpr88 is an orphan G protein-coupled receptor highly expressed in the striatum, a region important for motor control and learning. We developed a mouse lacking this receptor (genotype Gpr88Cre/Cre) by replacing most of the open-reading-frame of the Gpr88 gene with Cre recombinase. When comparing the homozygous knockouts against wild-type mice (Gpr88+/+), we have observed that knockout mice are hyperactive, present motor deficits and impaired cue-based learning. However, the signaling pathways downstream of Gpr88 are unknown. To identify putative downstream factors we designed a microarray experiment to identify gene expression changes in the striata of animals lacking Gpr88.

ORGANISM(S): Mus musculus

SUBMITTER: Albert Quintana

PROVIDER: E-MTAB-1282 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Lack of GPR88 enhances medium spiny neuron activity and alters motor- and cue-dependent behaviors.

Quintana Albert A Sanz Elisenda E Wang Wengang W Storey Granville P GP Güler Ali D AD Wanat Matthew J MJ Roller Bryan A BA La Torre Anna A Amieux Paul S PS McKnight G Stanley GS Bamford Nigel S NS Palmiter Richard D RD

Nature neuroscience 20121014 11

The striatum regulates motor control, reward and learning. Abnormal function of striatal GABAergic medium spiny neurons (MSNs) is believed to contribute to the deficits in these processes that are observed in many neuropsychiatric diseases. The orphan G protein-coupled receptor GPR88 is robustly expressed in MSNs and is regulated by neuropharmacological drugs, but its contribution to MSN physiology and behavior is unclear. We found that, in the absence of GPR88, MSNs showed increased glutamaterg ...[more]

PMID: 23064379

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