{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Orlandi C"],"funding":["NIDA NIH HHS","NIMH NIH HHS","U.S. Department of Health & Human Services | NIH | National Institute of Mental Health","U.S. Department of Health & Human Services | NIH | National Institute of Mental Health (NIMH)"],"pagination":["642-653"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6333837"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["44(3)"],"pubmed_abstract":["Affective disorders arise from abnormal responses of the brain to prolonged exposure to challenging environmental stimuli. Recent work identified the orphan receptor GPR158 as a molecular link between chronic stress and depression. Here we reveal a non-canonical mechanism by which GPR158 exerts its effects on stress-induced depression by the complex formation with Regulator of G protein Signaling 7 (RGS7). Chronic stress promotes membrane recruitment of RGS7 via GPR158 in the medial prefrontal cortex (mPFC). The resultant complex suppresses homeostatic regulation of cAMP by inhibitory GPCRs in the region. Accordingly, RGS7 loss in mice induces an antidepressant-like phenotype and resiliency to stress, whereas its restoration within the mPFC is sufficient to rescue this phenotype in a GPR15"],"journal":["Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology"],"pubmed_title":["Homeostatic cAMP regulation by the RGS7 complex controls depression-related behaviors."],"pmcid":["PMC6333837"],"funding_grant_id":["MH105482","R01 MH105482","F32 DA041207","K02 DA026405"],"pubmed_authors":["Martemyanov KA","Orlandi C","Muntean BS","Song C","Sutton LP"],"additional_accession":[]},"is_claimable":false,"name":"Homeostatic cAMP regulation by the RGS7 complex controls depression-related behaviors.","description":"Affective disorders arise from abnormal responses of the brain to prolonged exposure to challenging environmental stimuli. Recent work identified the orphan receptor GPR158 as a molecular link between chronic stress and depression. Here we reveal a non-canonical mechanism by which GPR158 exerts its effects on stress-induced depression by the complex formation with Regulator of G protein Signaling 7 (RGS7). Chronic stress promotes membrane recruitment of RGS7 via GPR158 in the medial prefrontal cortex (mPFC). The resultant complex suppresses homeostatic regulation of cAMP by inhibitory GPCRs in the region. Accordingly, RGS7 loss in mice induces an antidepressant-like phenotype and resiliency to stress, whereas its restoration within the mPFC is sufficient to rescue this phenotype in a GPR15","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Feb","modification":"2025-04-21T15:03:10.89Z","creation":"2025-04-21T15:03:10.89Z"},"accession":"S-EPMC6333837","cross_references":{"pubmed":["30546127"],"doi":["10.1038/s41386-018-0238-y"]}}