title: Abnormal glutamate release in aged BTBR mouse model of autism.
abstract: Autism is a neurodevelopmental disorder characterized by abnormal reciprocal social interactions, communication deficits, and repetitive behaviors with restricted interests. Most of the available research on autism is focused on children and young adults and little is known about the pathological alternation of autism in older adults. In order to investigate the neurobiological alternation of autism in old age stage, we compared the morphology and synaptic function of excitatory synapses between the BTBR mice with low level sociability and B6 mice with high level sociability. The results revealed that the number of excitatory synapse colocalized with pre- and post-synaptic marker was not different between aged BTBR and B6 mice. The aged BTBR mice had a normal structure of dendritic spine and the expression of Shank3 protein in the brain as well as that in B6 mice. The baseline and KCl-evoked glutamate release from the cortical synaptoneurosome in aged BTBR mice was lower than that in aged B6 mice. Overall, the data indicate that there is a link between disturbances of the glutamate transmission and autism. These findings provide new evidences for the hypothesis of excitation/inhibition imbalance in autism. Further work is required to determine the cause of this putative abnormality.
authors.affiliation: Central Laboratory, Shanxi Provincial People's Hospital, Affiliate of Shanxi Medical University Taiyuan, China.
authors.forename: Hongen
authors.initials: H
authors.lastname: Wei
authors.affiliation: Central Laboratory, Shanxi Provincial People's Hospital, Affiliate of Shanxi Medical University Taiyuan, China.
authors.forename: Caiyun
authors.initials: C
authors.lastname: Ding
authors.affiliation: Central Laboratory, Shanxi Provincial People's Hospital, Affiliate of Shanxi Medical University Taiyuan, China.
authors.forename: Guorong
authors.initials: G
authors.lastname: Jin
authors.affiliation: Central Laboratory, Shanxi Provincial People's Hospital, Affiliate of Shanxi Medical University Taiyuan, China.
authors.forename: Haizhen
authors.initials: H
authors.lastname: Yin
authors.affiliation: Central Laboratory, Shanxi Provincial People's Hospital, Affiliate of Shanxi Medical University Taiyuan, China.
authors.forename: Jianrong
authors.initials: J
authors.lastname: Liu
authors.affiliation: Department of Neurology, Shanxi Provincial People's Hospital, Affiliate of Shanxi Medical University Taiyuan, China.
authors.forename: Fengyun
authors.initials: F
authors.lastname: Hu
mesh_terms: D000818:Animals; D001321:Autistic Disorder / Q000235:genetics / Q000378:metabolism* / Q000503:physiopathology / Q000523:psychology; D001522:Behavior, Animal; D002540:Cerebral Cortex / Q000378:metabolism* / Q000503:physiopathology; D049229:Dendritic Spines / Q000378:metabolism; D019706:Excitatory Postsynaptic Potentials; D020022:Genetic Predisposition to Disease; D018698:Glutamic Acid / Q000378:metabolism*; D008810:Mice, Inbred C57BL; D008840:Microfilament Proteins; D009419:Nerve Tissue Proteins / Q000378:metabolism; D010641:Phenotype; D012919:Social Behavior; D009435:Synaptic Transmission
chemical_list: D008840:Microfilament Proteins; D009419:Nerve Tissue Proteins; C492356:Shank3 protein, mouse; D018698:Glutamic Acid
keywords: Autism; BTBR mice; aging; excitatory synapse; glutamate release