Open Access Highly Accessed Research article

The Adhesion GPCR GPR125 is specifically expressed in the choroid plexus and is upregulated following brain injury

Chris Pickering1*, Maria Hägglund1, Joanna Szmydynger-Chodobska3, Fernanda Marques4, Joana A Palha4, Linn Waller1, Adam Chodobski3, Robert Fredriksson1, Malin C Lagerström12 and Helgi B Schiöth1

Author Affiliations

1 Uppsala University, Department of Neuroscience, Functional Pharmacology, BMC, Box 593, SE-75124, Uppsala, Sweden

2 Uppsala University, Department of Neuroscience, Division of Developmental Genetics, BMC, Box 587, SE-75124, Uppsala, Sweden

3 The Warren Alpert Medical School of Brown University, Department of Clinical Neurosciences, Aldrich Building 405, 593 Eddy Street, Providence, RI 02903, USA

4 University of Minho, Life and Health Sciences Research Institute (ICVS), School of Health Sciences, Campus Gualtar, 4710-057, Braga, Portugal

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BMC Neuroscience 2008, 9:97  doi:10.1186/1471-2202-9-97

Published: 3 October 2008



GPR125 belongs to the family of Adhesion G protein-coupled receptors (GPCRs). A single copy of GPR125 was found in many vertebrate genomes. We also identified a Drosophila sequence, DmCG15744, which shares a common ancestor with the entire Group III of Adhesion GPCRs, and also contains Ig, LRR and HBD domains which were observed in mammalian GPR125.


We found specific expression of GPR125 in cells of the choroid plexus using in situ hybridization and protein-specific antibodies and combined in situ/immunohistochemistry co-localization using cytokeratin, a marker specific for epithelial cells. Induction of inflammation by LPS did not change GPR125 expression. However, GPR125 expression was transiently increased (almost 2-fold) at 4 h after traumatic brain injury (TBI) followed by a decrease (approximately 4-fold) from 2 days onwards in the choroid plexus as well as increased expression (2-fold) in the hippocampus that was delayed until 1 day after injury.


These findings suggest that GPR125 plays a functional role in choroidal and hippocampal response to injury.