Asset Details
Do you wish to reserve the book?
Sensorimotor gating abnormalities in young males with fragile X syndrome and Fmr1-knockout mice
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?
Sensorimotor gating abnormalities in young males with fragile X syndrome and Fmr1-knockout mice
Do you wish to request the book?
Sensorimotor gating abnormalities in young males with fragile X syndrome and Fmr1-knockout mice
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
Sensorimotor gating abnormalities in young males with fragile X syndrome and Fmr1-knockout mice
2004
Overview
Fragile X syndrome (FXS) is the most common single gene (
FMR1
) disorder affecting cognitive and behavioral function in humans. This syndrome is characterized by a cluster of abnormalities including lower IQ, attention deficits, impairments in adaptive behavior and increased incidence of autism. Here, we show that young males with FXS have profound deficits in prepulse inhibition (PPI), a basic marker of sensorimotor gating that has been extensively studied in rodents. Importantly, the magnitude of the PPI impairments in the fragile X children predicted the severity of their IQ, attention, adaptive behavior and autistic phenotypes. Additionally, these measures were highly correlated with each other, suggesting that a shared mechanism underlies this complex phenotypic cluster. Studies in
Fmr1
-knockout mice also revealed sensorimotor gating and learning abnormalities. However, PPI and learning were enhanced rather than reduced in the mutants. Therefore, these data show that mutations of the
FMR1
gene impact equivalent processes in both humans and mice. However, since these phenotypic changes are opposite in direction, they also suggest that murine compensatory mechanisms following loss of
FMR1
function differ from those in humans.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ Animals
/ Autism
/ Biological and medical sciences
/ Child
/ Child Behavior Disorders - genetics
/ Child Development Disorders, Pervasive - genetics
/ Cognition Disorders - genetics
/ Conditioning (Psychology) - physiology
/ Fragile X Mental Retardation Protein
/ Fragile X Syndrome - genetics
/ Fragile X Syndrome - physiopathology
/ Humans
/ Ion Channel Gating - genetics
/ Ion Channel Gating - physiology
/ Male
/ Medicine
/ Mice
/ Mutation
/ Nerve Tissue Proteins - genetics
/ Nerve Tissue Proteins - physiology
/ Neural Inhibition - genetics
/ Neural Inhibition - physiology
/ RNA-Binding Proteins - genetics
