ArticleTranslational psychiatry2015
LPA signaling initiates schizophrenia-like brain and behavioral changes in a mouse model of prenatal brain hemorrhage.
Article in Translational psychiatry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 48 citations in OpenAlex.
- Decoding lysophosphatidic acid signaling in physiology and disease: mapping the multimodal and multinodal signaling networks.Signal transduction and targeted therapy · 2025Review
- Dysregulation of myelination-related genes in schizophrenia.Journal of neurochemistry · 2024Review
- G protein-biased LPAR1 agonism of prototypic antidepressants: Implication in the identification of novel therapeutic target for depression.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024Article
- LPA1 receptors in the lateral habenula regulate negative affective states associated with alcohol withdrawal.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023Article
- Maternal immune activation leads to defective brain-blood vessels and intracerebral hemorrhages in male offspring.The EMBO journal · 2022Article
- Neurological consequences of neurovascular unit and brain vasculature damages: potential risks for pregnancy infections and COVID-19-babies.The FEBS journal · 2022Review
- Sex Differences in Plasma Lysophosphatidic Acid Species in Patients with Alcohol and Cocaine Use Disorders.Brain sciences · 2022Article
- Reduced Cerebrospinal Fluid Levels of Lysophosphatidic Acid Docosahexaenoic Acid in Patients With Major Depressive Disorder and Schizophrenia.The international journal of neuropsychopharmacology · 2021Article
- Generation of an Lpar1-EGFP Fusion Knock-in Transgenic Mouse Line.Cell biochemistry and biophysics · 2021Article
- GABAergic deficits in absence of LPABrain structure & function · 2021Article
- Lysophosphatidic Acid Signalling in Nervous System Development and Function.Neuromolecular medicine · 2021Review
- Dual Role of Lysophosphatidic Acid Receptor 2 (LPAFrontiers in cellular neuroscience · 2021Article
- Altered cleavage plane orientation with increased genomic aneuploidy produced by receptor-mediated lysophosphatidic acid (LPA) signaling in mouse cerebral cortical neural progenitor cells.Molecular brain · 2020Article
- Potential association of plasma lysophosphatidic acid (LPA) species with cognitive impairment in abstinent alcohol use disorders outpatients.Scientific reports · 2020Article
- Conditional Lpar1 gene targeting identifies cell types mediating neuropathic pain.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Pleotropic Roles of Autotaxin in the Nervous System Present Opportunities for the Development of Novel Therapeutics for Neurological Diseases.Molecular neurobiology · 2020Review
- S1PBiomolecules & therapeutics · 2019Article
- Expression analysis and genotyping of DGKZ: a GWAS-derived risk gene for schizophrenia.Molecular biology reports · 2019Article
- LPADevelopmental dynamics : an official publication of the American Association of Anatomists · 2019Article
- Effects of the LPAFrontiers in molecular neuroscience · 2019Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Genetic, environmental and neurodevelopmental factors are thought to underlie the onset of neuropsychiatric disorders such as schizophrenia. How these risk factors collectively contribute to pathology is unclear. Here, we present a mouse model of prenatal intracerebral hemorrhage--an identified risk factor for schizophrenia--using a serum-exposure paradigm. This model exhibits behavioral, neurochemical and schizophrenia-related gene expression alterations in adult females. Behavioral alterations in amphetamine-induced locomotion, prepulse inhibition, thigmotaxis and social interaction--in addition to increases in tyrosine hydroxylase-positive dopaminergic cells in the substantia nigra and ventral tegmental area and decreases in parvalbumin-positive cells in the prefrontal cortex--were induced upon prenatal serum exposure. Lysophosphatidic acid (LPA), a lipid component of serum, was identified as a key molecular initiator of schizophrenia-like sequelae induced by serum. Prenatal exposure to LPA alone phenocopied many of the schizophrenia-like alterations seen in the serum model, whereas pretreatment with an antagonist against the LPA receptor subtype LPA1 prevented many of the behavioral and neurochemical alterations. In addition, both prenatal serum and LPA exposure altered the expression of many genes and pathways related to schizophrenia, including the expression of Grin2b, Slc17a7 and Grid1. These findings demonstrate that aberrant LPA receptor signaling associated with fetal brain hemorrhage may contribute to the development of some neuropsychiatric disorders.
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