{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhao S"],"funding":["U.S. Department of Health &amp; Human Services | NIH | National Institute of Neurological Disorders and Stroke","NIA NIH HHS","NIEHS NIH HHS","U.S. Department of Health &amp; Human Services | NIH | National Institute of Environmental Health Sciences","NINDS NIH HHS"],"pagination":["2857-2871"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10906107"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["28(7)"],"pubmed_abstract":["Chemogenetic approaches using Designer Receptors Exclusively Activated by Designer Drugs (DREADD, a family of engineered GPCRs) were recently employed in microglia. Here, we used Cx3cr1<sup>CreER/+</sup>:R26<sup>hM4Di/+</sup> mice to express Gi-DREADD (hM4Di) on CX3CR1<sup>+</sup> cells, comprising microglia and some peripheral immune cells, and found that activation of hM4Di on long-lived CX3CR1<sup>+</sup> cells induced hypolocomotion. Unexpectedly, Gi-DREADD-induced hypolocomotion was preserved when microglia were depleted. Consistently, specific activation of microglial hM4Di cannot induce hypolocomotion in Tmem119<sup>CreER/+</sup>:R26<sup>hM4Di/+</sup> mice. Flow cytometric and histological analysis showed hM4Di expression in peripheral immune cells, which may be responsible for the hypolocomotion. Nevertheless, depletion of splenic macrophages, hepatic macrophages, or CD4<sup>+</sup> T cells did not affect Gi-DREADD-induced hypolocomotion. Our study demonstrates that rigorous data analysis and interpretation are needed when using Cx3cr1<sup>CreER/+</sup> mouse line to manipulate microglia."],"journal":["Molecular psychiatry"],"pubmed_title":["Chemogenetic manipulation of CX3CR1<sup>+</sup> cells transiently induces hypolocomotion independent of microglia."],"pmcid":["PMC10906107"],"funding_grant_id":["R35NS132326","R35 NS132326","R01 ES033892","R01ES033892","K99 NS126417","K99NS126417","R01 NS110949","RF1 AG082314"],"pubmed_authors":["Zheng J","Umpierre AD","Dheer A","Zhao S","Richardson JR","Xie M","Johnson AJ","Ayasoufi K","Wang L","Parusel S","Wu LJ"],"additional_accession":[]},"is_claimable":false,"name":"Chemogenetic manipulation of CX3CR1<sup>+</sup> cells transiently induces hypolocomotion independent of microglia.","description":"Chemogenetic approaches using Designer Receptors Exclusively Activated by Designer Drugs (DREADD, a family of engineered GPCRs) were recently employed in microglia. Here, we used Cx3cr1<sup>CreER/+</sup>:R26<sup>hM4Di/+</sup> mice to express Gi-DREADD (hM4Di) on CX3CR1<sup>+</sup> cells, comprising microglia and some peripheral immune cells, and found that activation of hM4Di on long-lived CX3CR1<sup>+</sup> cells induced hypolocomotion. Unexpectedly, Gi-DREADD-induced hypolocomotion was preserved when microglia were depleted. Consistently, specific activation of microglial hM4Di cannot induce hypolocomotion in Tmem119<sup>CreER/+</sup>:R26<sup>hM4Di/+</sup> mice. Flow cytometric and histological analysis showed hM4Di expression in peripheral immune cells, which may be responsible for the hypolocomotion. Nevertheless, depletion of splenic macrophages, hepatic macrophages, or CD4<sup>+</sup> T cells did not affect Gi-DREADD-induced hypolocomotion. Our study demonstrates that rigorous data analysis and interpretation are needed when using Cx3cr1<sup>CreER/+</sup> mouse line to manipulate microglia.","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Jul","modification":"2026-05-29T17:29:35.843Z","creation":"2026-04-08T05:37:41.685Z"},"accession":"S-EPMC10906107","cross_references":{"pubmed":["37365239"],"doi":["10.1038/s41380-023-02128-6"]}}