Enhanced Tau Protein Translation by Hyper-Excitation

Tau is a microtubule-associated protein, localizing mainly in the axon of mature neurons. Phenotypic analysis of knockout mice has revealed an impairment of synaptic plasticity but without gross changes in brain morphology. Since we previously described the presence of tau mRNA in the somatodendriti...

Full description

Saved in:
Bibliographic Details
Published inFrontiers in aging neuroscience Vol. 11; p. 322
Main Authors Kobayashi, Shunsuke, Tanaka, Toru, Soeda, Yoshiyuki, Takashima, Akihiko
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Research Foundation 20.11.2019
Frontiers Media S.A
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Tau is a microtubule-associated protein, localizing mainly in the axon of mature neurons. Phenotypic analysis of knockout mice has revealed an impairment of synaptic plasticity but without gross changes in brain morphology. Since we previously described the presence of tau mRNA in the somatodendritic compartment, including the postsynapse, and demonstrated that it could be locally translated in response to glutamate, it appears that the regulated translation of synaptic tau can have a direct impact on synaptic function. Using SH-SY5Y cells, we herein confirm that glutamate dose-dependently regulates the translation of tau protein without altering tau mRNA levels. This is supported by the finding that cycloheximide blocks glutamate-stimulated increases in tau protein levels. Our observation that neural excitation can directly upregulate tau mRNA translation helps explain the pathological accumulation of tau in the somatodendrite.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
Edited by: Miguel Medina, Network Center for Biomedical Research in Neurodegenerative Diseases (CIBERNED), Spain
Reviewed by: Emmanuel Planel, Laval University, Canada; Jesus Avila, Autonomous University of Madrid, Spain
ISSN:1663-4365
1663-4365
DOI:10.3389/fnagi.2019.00322