The implication of AMPA receptor in synaptic plasticity impairment and intellectual disability in fragile X syndrome

Title:

The implication of AMPA receptor in synaptic plasticity impairment and intellectual disability in fragile X syndrome

Creator:

Cheng, Gui-Rong, Li, Xiang-Yu, Xiang, Ya-Die, Liu, Dan, McClintock, Shawn M., and Zeng, Yan

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:23b7b2bd-9c28-45e6-b472-a0c437348cf8
uuid:23b7b2bd-9c28-45e6-b472-a0c437348cf8

Subject:

fragile X syndrome, intellectual disability, AMPA receptors, synaptic plasticity, and learning and memory

Type:

article, model:article, and TEXT

Description:

Fragile X syndrome (FXS) is the most frequently inherited form of intellectual disability and prevalent single-gene cause of autism. A priority of FXS research is to determine the molecular mechanisms underlying the cognitive and social functioning impairments in humans and the FXS mouse model. Glutamate ionotropic alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptors (AMPARs) mediate a majority of fast excitatory neurotransmission in the central nervous system and are critically important for nearly all aspects of brain function, including neuronal development, synaptic plasticity, and learning and memory. Both preclinical and clinical studies have indicated that expression, trafficking, and functions of AMPARs are altered and result in altered synapse development and plasticity, cognitive impairment, and poor mental health in FXS. In this review, we discuss the contribution of AMPARs to disorders of FXS by highlighting recent research advances with a specific focus on change in AMPARs expression, trafficking, and dependent synaptic plasticity. Since changes in synaptic strength underlie the basis of learning, development, and disease, we suggest that the current knowledge base of AMPARs has reached a unique point to permit a comprehensive re-evaluation of their roles in FXS.

Language:

English

Rights:

http://creativecommons.org/publicdomain/mark/1.0/
policy:public

Source:

Physiological research | 2017 Volume:66 | Number:5

Harvested from:

CDK

Metadata only:

false