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Long-term Depression01:03

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Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
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Related Experiment Video

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Evaluation of Synaptic Multiplicity Using Whole-cell Patch-clamp Electrophysiology
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Published on: April 23, 2019

DGKι regulates presynaptic release during mGluR-dependent LTD.

Jinhee Yang1, Jinsoo Seo, Ramya Nair

  • 1Department of Biological Sciences, National Creative Research Initiative Center for Synaptogenesis, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, Korea.

The EMBO Journal
|December 2, 2010
PubMed
Summary

Diacylglycerol kinase ι (DGKι) is localized to synapses via PSD-95 proteins, regulating presynaptic neurotransmitter release. DGKι deficiency impairs metabotropic glutamate receptor-dependent long-term depression in neonatal mice.

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Last Updated: Jun 6, 2026

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12:47

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cell Biology

Background:

  • Diacylglycerol (DAG) acts as a crucial lipid second messenger in cellular signaling.
  • Diacylglycerol kinases (DGKs) terminate DAG signaling by converting DAG to phosphatidic acid (PA).
  • The neuronal synapse is a key location for DAG production and function, but DGK targeting mechanisms remain unclear.

Purpose of the Study:

  • To investigate the synaptic localization mechanisms of DGKι.
  • To elucidate the presynaptic role of DGKι in neurotransmitter release and synaptic plasticity.
  • To understand the regulation of DGKι function in metabotropic glutamate receptor-dependent long-term depression (mGluR-LTD).

Main Methods:

  • Co-immunoprecipitation assays to study protein interactions.
  • Confocal microscopy for subcellular localization studies.
  • Electrophysiological recordings in DGKι-deficient mice to assess synaptic function.
  • Pharmacological inhibition of protein kinase C.

Main Results:

  • Postsynaptic density (PSD)-95 family proteins interact with and facilitate the synaptic localization of DGKι.
  • DGKι functions presynaptically, unlike its postsynaptic relative DGKζ.
  • DGKι deficiency in mice results in increased presynaptic release probability and impaired mGluR-LTD at neonatal stages.
  • Inhibition of protein kinase C rescues presynaptic release probability and mGluR-LTD in DGKι-deficient synapses.

Conclusions:

  • DGKι synaptic localization is mediated by PSD-95 family proteins.
  • DGKι plays a critical role in regulating presynaptic DAG signaling and neurotransmitter release during mGluR-LTD.
  • These findings reveal a novel presynaptic function for DGKι in synaptic plasticity.