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DGKi regulates presynaptic release during mGluR-dependent LTD

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dc.contributor.authorYang, Jinhee-
dc.contributor.authorSeo, Jinsoo-
dc.contributor.authorNair, Ramya-
dc.contributor.authorHan, Seungnam-
dc.contributor.authorJang, Seil-
dc.contributor.authorKim, Karam-
dc.contributor.authorHan, Kihoon-
dc.contributor.authorPaik, Sang Kyoo-
dc.contributor.authorChoi, Jeonghoon-
dc.contributor.authorLee, Seunghoon-
dc.contributor.authorBae, Yong Chul-
dc.contributor.authorTopham, Matthew K-
dc.contributor.authorPrescott, Stephen M-
dc.contributor.authorRhee, Jeong-Seop-
dc.contributor.authorChoi, Se-Young-
dc.contributor.authorKim, Eunjoon-
dc.date.accessioned2011-10-17T01:38:33Z-
dc.date.available2011-10-17T01:38:33Z-
dc.date.issued2011-01-
dc.identifier.citationThe EMBO Journal 30:165-180en
dc.identifier.issn0261-4189-
dc.identifier.urihttps://hdl.handle.net/10371/74187-
dc.description.abstractDiacylglycerol (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.en
dc.description.sponsorshipThis work was supported by the NIH R01-CA95463 grant (to MKT), the Neuroscience Program (to S-YC; 2009-0081468), and the
National Creative Research Initiative Program of the Korean Ministry of Education, Science, and Technology (to EK).
en
dc.language.isoenen
dc.publisherNature Publishing Groupen
dc.subjectdiacylglycerol kinaseen
dc.subjectlong-term depressionen
dc.subjectmetabotropic glutamate receptorsen
dc.subjectphospholipase Cen
dc.subjectPSD-95en
dc.titleDGKi regulates presynaptic release during mGluR-dependent LTDen
dc.typeArticleen
dc.contributor.AlternativeAuthor양진희-
dc.contributor.AlternativeAuthor서진수-
dc.contributor.AlternativeAuthor한승남-
dc.contributor.AlternativeAuthor장세일-
dc.contributor.AlternativeAuthor김가람-
dc.contributor.AlternativeAuthor한기훈-
dc.contributor.AlternativeAuthor백상규-
dc.contributor.AlternativeAuthor최정훈-
dc.contributor.AlternativeAuthor이승훈-
dc.contributor.AlternativeAuthor배용철-
dc.contributor.AlternativeAuthor이정섭-
dc.contributor.AlternativeAuthor최세영-
dc.contributor.AlternativeAuthor김은준-
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