Publications
Detailed Information
DGKi regulates presynaptic release during mGluR-dependent LTD
Cited 0 time in
Web of Science
Cited 0 time in Scopus
- Authors
- Issue Date
- 2011-01
- Publisher
- Nature Publishing Group
- Citation
- The EMBO Journal 30:165-180
- Keywords
- diacylglycerol kinase ; long-term depression ; metabotropic glutamate receptors ; phospholipase C ; PSD-95
- Abstract
- Diacylglycerol (DAG) is an important lipid second messenger. DAG signalling is terminated by conversion of DAG to phosphatidic acid (PA) by diacylglycerol kinases (DGKs). The neuronal synapse is a major site of DAG production and action; however, how DGKs are targeted to subcellular sites of DAG generation is largely unknown. We report here that postsynaptic density (PSD)-95 family proteins interact with and promote synaptic localization of DGKl. In addition, we establish that DGKl acts presynaptically, a function that contrasts with the known postsynaptic function of DGKl, a close relative of DGKl. Deficiency of DGKl in mice does not affect dendritic spines, but leads to a small increase in presynaptic release probability. In addition, DGKl-/- synapses show a reduction in metabotropic glutamate receptor-dependent long-term depression (mGluR-LTD) at neonatal (∼2 weeks) stages that involve suppression of a decrease in presynaptic release probability. Inhibition of protein kinase C normalizes presynaptic release probability and mGluR-LTD at DGKl-/- synapses. These results suggest that DGKl requires PSD-95 family proteins for synaptic localization and regulates presynaptic DAG signalling and neurotransmitter release during mGluR-LTD.
- ISSN
- 0261-4189
- Language
- English
- Files in This Item:
- There are no files associated with this item.
Item View & Download Count
Items in S-Space are protected by copyright, with all rights reserved, unless otherwise indicated.