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Related Concept Videos

Long-term Potentiation01:25

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

Updated: Aug 26, 2025

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Long-term potentiation reconstituted with an artificial TARP/PSD-95 complex.

Anagh Sinha Ravi1, Menglong Zeng2, Xudong Chen2

  • 1Department of Cellular and Molecular Pharmacology, University of California at San Francisco, San Francisco, CA, USA.

Cell Reports
|October 12, 2022
PubMed
Summary

The transmembrane AMPAR regulatory protein (TARP) and PSD-95 interaction is essential for AMPA receptor trafficking and long-term potentiation (LTP). Engineered binding partners rescued synaptic transmission and LTP, confirming this complex

Keywords:
AMPA receptor traffickingAMPARCP: NeuroscienceGluA1LTPMAGUKPSD-95TARPpostsynaptic densitysynaptic transmission

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Synaptic Plasticity

Background:

  • AMPA receptor (AMPAR) trafficking is crucial for long-term potentiation (LTP) in excitatory synapses.
  • The precise molecular mechanisms governing AMPAR trafficking and LTP remain incompletely understood.
  • PSD-95 is hypothesized to capture AMPARs through interactions with transmembrane AMPAR regulatory proteins (TARPs).

Purpose of the Study:

  • To investigate whether the TARP/PSD-95 interaction is a fundamental component of AMPAR trafficking and LTP.
  • To determine the necessity of this specific interaction for synaptic function and plasticity.

Main Methods:

  • Engineered artificial binding partners designed to mimic or disrupt the TARP/PSD-95 interaction.
  • Biochemical assays to confirm binding capabilities of engineered partners.
  • Electrophysiological recordings to assess basal synaptic transmission and LTP in the presence of engineered partners.

Main Results:

  • Individually, engineered binding partners were biochemically inactive and functionally deficient.
  • Co-expression of engineered partners restored the TARP/PSD-95 binding interaction.
  • Restored binding rescued both basal synaptic transmission and long-term potentiation (LTP).

Conclusions:

  • The TARP/PSD-95 complex is an essential molecular interaction for AMPAR trafficking.
  • This interaction is critical for the mechanisms underlying synaptic plasticity, including LTP.
  • The findings establish a core molecular requirement for synaptic potentiation.