TY - JOUR
T1 - The implication of AMPA receptor in synaptic plasticity impairment and intellectual disability in fragile X syndrome
AU - Cheng, Gui Rong
AU - Li, Xiang Yu
AU - Xiang, Ya Die
AU - Liu, Dan
AU - Mcclintock, Shawn M.
AU - Zeng, Yan
N1 - Funding Information:
This work was supported by the National Natural Science Foundation of China (grant 31271199 to Dr. Yan Zeng), and the National Natural Science Foundation of China (grant 81571095 to Dr. Yan Zeng). It was also supported by the Students' Science and Technology Innovation Fund from Wuhan University of Science and Technology (15ZRA161 to Yadie Xiang) and Students' Innovative Entrepreneurial Training Plan from Hubei Province (201510488044 to Xiangyu Li).
PY - 2017
Y1 - 2017
N2 - 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.
AB - 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.
KW - AMPA receptors
KW - Fragile X syndrome
KW - Intellectual disability
KW - Learning and memory
KW - Synaptic plasticity
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U2 - 10.33549/physiolres.933473
DO - 10.33549/physiolres.933473
M3 - Review article
C2 - 28730825
AN - SCOPUS:85037045951
VL - 66
SP - 715
EP - 727
JO - Physiological Research
JF - Physiological Research
SN - 0862-8408
IS - 5
ER -