UMMS Affiliation

Program in Molecular Medicine

Date

3-12-2015

Document Type

Article

Medical Subject Headings

Animals; Biomarkers; Cerebral Cortex; Enzyme Activation; Exocytosis; Female; Glutamic Acid; Male; Mice; Mice, Knockout; Mitogen-Activated Protein Kinase 9; Phosphorylation; Presynaptic Terminals; Receptors, AMPA; Receptors, N-Methyl-D-Aspartate; Synaptosomes; Time-Lapse Imaging

Disciplines

Biochemistry | Cell Biology | Cellular and Molecular Physiology | Molecular Biology

Abstract

Activation of c-Jun N-terminal kinase (JNK) signaling pathway is a critical step for neuronal death occurring in several neurological conditions. JNKs can be activated via receptor tyrosine kinases, cytokine receptors, G-protein coupled receptors and ligand-gated ion channels, including the NMDA glutamate receptors. While JNK has been generally associated with postsynaptic NMDA receptors, its presynaptic role remains largely unexplored. Here, by means of biochemical, morphological and functional approaches, we demonstrate that JNK and its scaffold protein JIP1 are also expressed at the presynaptic level and that the NMDA-evoked glutamate release is controlled by presynaptic JNK-JIP1 interaction. Moreover, using knockout mice for single JNK isoforms, we proved that JNK2 is the essential isoform in mediating this presynaptic event. Overall the present findings unveil a novel JNK2 localization and function, which is likely to play a role in different physiological and pathological conditions.

Rights and Permissions

Citation: Sci Rep. 2015 Mar 12;5:9035. doi: 10.1038/srep09035. Link to article on publisher's site

Comments

This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder in order to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

Related Resources

Link to Article in PubMed

PubMed ID

25762148

Creative Commons License

Creative Commons Attribution 4.0 License
This work is licensed under a Creative Commons Attribution 4.0 License.

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