{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Santos-Silva T"],"funding":["São Paulo Research Foundation","Alexander von Humboldt Foundation","Coordination for the Improvement of Higher Education Personnel-Brazil"],"pagination":["210-223"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10754178"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["50(1)"],"pubmed_abstract":["<h4>Background</h4>Consistent with postmortem findings in patients, most animal models for schizophrenia (SCZ) present abnormal levels of parvalbumin (PV), a marker of fast-spiking GABAergic interneurons, in the prefrontal cortex (PFC) and hippocampus (HIP). However, there are discrepancies in the literature. PV reductions lead to a functional loss of PV interneurons, which is proposed to underly SCZ symptoms. Given its complex etiology, different categories of animal models have been developed to study SCZ, which may distinctly impact PV levels in rodent brain areas.<h4>Study design</h4>We performed a quantitative meta-analysis on PV-positive cell number/density and expression levels in the PFC and HIP of animal models for SCZ based on pharmacological, neurodevelopmental, and genetic mani"],"journal":["Schizophrenia bulletin"],"pubmed_title":["Prefrontal and Hippocampal Parvalbumin Interneurons in Animal Models for Schizophrenia: A Systematic Review and Meta-analysis."],"pmcid":["PMC10754178"],"funding_grant_id":["19/24591-4","#88887.334572/2019-00"],"pubmed_authors":["de Oliveira CL","Dos Santos Fabris D","Gomes FV","Santos-Silva T","Guimaraes FS"],"additional_accession":[]},"is_claimable":false,"name":"Prefrontal and Hippocampal Parvalbumin Interneurons in Animal Models for Schizophrenia: A Systematic Review and Meta-analysis.","description":"<h4>Background</h4>Consistent with postmortem findings in patients, most animal models for schizophrenia (SCZ) present abnormal levels of parvalbumin (PV), a marker of fast-spiking GABAergic interneurons, in the prefrontal cortex (PFC) and hippocampus (HIP). However, there are discrepancies in the literature. PV reductions lead to a functional loss of PV interneurons, which is proposed to underly SCZ symptoms. Given its complex etiology, different categories of animal models have been developed to study SCZ, which may distinctly impact PV levels in rodent brain areas.<h4>Study design</h4>We performed a quantitative meta-analysis on PV-positive cell number/density and expression levels in the PFC and HIP of animal models for SCZ based on pharmacological, neurodevelopmental, and genetic mani","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jan","modification":"2025-04-19T13:52:58.412Z","creation":"2025-04-19T13:52:58.412Z"},"accession":"S-EPMC10754178","cross_references":{"pubmed":["37584417"],"doi":["10.1093/schbul/sbad123"]}}