Asset Details
Do you wish to reserve the book?
Fabp7 maps to a quantitative trait locus for a schizophrenia endophenotype
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Fabp7 maps to a quantitative trait locus for a schizophrenia endophenotype
Do you wish to request the book?
Fabp7 maps to a quantitative trait locus for a schizophrenia endophenotype
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Fabp7 maps to a quantitative trait locus for a schizophrenia endophenotype
2007
Overview
Deficits in prepulse inhibition (PPI) are a biological marker for schizophrenia. To unravel the mechanisms that control PPI, we performed quantitative trait loci (QTL) analysis on 1,010 F2 mice derived by crossing C57BL/6 (B6) animals that show high PPI with C3H/He (C3) animals that show low PPI. We detected six major loci for PPI, six for the acoustic startle response, and four for latency to response peak, some of which were sex-dependent. A promising candidate on the Chromosome 10-QTL was Fabp7 (fatty acid binding protein 7, brain), a gene with functional links to the N-methyl-D-aspartic acid (NMDA) receptor and expression in astrocytes. Fabp7-deficient mice showed decreased PPI and a shortened startle response latency, typical of the QTL's proposed effects. A quantitative complementation test supported Fabp7 as a potential PPI-QTL gene, particularly in male mice. Disruption of Fabp7 attenuated neurogenesis in vivo. Human FABP7 showed altered expression in schizophrenic brains and genetic association with schizophrenia, which were both evident in males when samples were divided by sex. These results suggest that FABP7 plays a novel and crucial role, linking the NMDA, neurodevelopmental, and glial theories of schizophrenia pathology and the PPI endophenotype, with larger or overt effects in males. We also discuss the results from the perspective of fetal programming.
Publisher
Public Library of Science,Public Library of Science (PLoS)
Subject
/ Chromosome Mapping - methods
/ Disease
/ Fatty Acid-Binding Protein 7
/ Fatty Acid-Binding Proteins - genetics
/ Fatty Acid-Binding Proteins - metabolism
/ Gene Expression Regulation, Developmental
/ Genetic Predisposition to Disease
/ Genetics
/ Genomes
/ Genomics
/ Humans
/ Males
/ Mice
/ Nerve Tissue Proteins - genetics
/ Nerve Tissue Proteins - metabolism
/ Proteins
/ Quantitative Trait Loci - genetics
/ Receptors, N-Methyl-D-Aspartate - genetics
/ Receptors, N-Methyl-D-Aspartate - metabolism
/ Rodents
