Asset Details
Do you wish to reserve the book?
Slitrk5 deficiency impairs corticostriatal circuitry and leads to obsessive-compulsive–like behaviors in 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?
Slitrk5 deficiency impairs corticostriatal circuitry and leads to obsessive-compulsive–like behaviors in mice
Do you wish to request the book?
Slitrk5 deficiency impairs corticostriatal circuitry and leads to obsessive-compulsive–like behaviors in 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
Slitrk5 deficiency impairs corticostriatal circuitry and leads to obsessive-compulsive–like behaviors in mice
2010
Overview
Individuals with obsessive-compulsive disorder (OCD) perform obsessive repetitive actions. Shahin Rafii and his colleagues show that mice lacking the gene
Slitrk5
show OCD-like behavioral phenotypes and have deficits in corticostriatal communication in the brain.
Obsessive-compulsive disorder (OCD) is a common psychiatric disorder defined by the presence of obsessive thoughts and repetitive compulsive actions, and it often encompasses anxiety and depressive symptoms
1
,
2
. Recently, the corticostriatal circuitry has been implicated in the pathogenesis of OCD
3
,
4
. However, the etiology, pathophysiology and molecular basis of OCD remain unknown. Several studies indicate that the pathogenesis of OCD has a genetic component
5
,
6
,
7
,
8
. Here we demonstrate that loss of a neuron-specific transmembrane protein, SLIT and NTRK-like protein-5 (Slitrk5), leads to OCD-like behaviors in mice, which manifests as excessive self-grooming and increased anxiety-like behaviors, and is alleviated by the selective serotonin reuptake inhibitor fluoxetine.
Slitrk5
−/−
mice show selective overactivation of the orbitofrontal cortex, abnormalities in striatal anatomy and cell morphology and alterations in glutamate receptor composition, which contribute to deficient corticostriatal neurotransmission. Thus, our studies identify Slitrk5 as an essential molecule at corticostriatal synapses and provide a new mouse model of OCD-like behaviors.
Publisher
Nature Publishing Group US,Nature Publishing Group
Subject
/ 692/420
/ Anatomy
/ Animals
/ Biomedical and Life Sciences
/ Compulsive Behavior - genetics
/ Etiology
/ Grooming
/ letter
/ Membrane Proteins - deficiency
/ Membrane Proteins - genetics
/ Mice
/ Neostriatum - physiopathology
/ Nerve Tissue Proteins - deficiency
/ Nerve Tissue Proteins - genetics
/ Obsessive-compulsive disorder
/ Obsessive-Compulsive Disorder - diagnosis
/ Proteins
/ Rodents
/ Synapses
