Related Experiment Video

Updated: Feb 21, 2026

A High-content Assay for Monitoring AMPA Receptor Trafficking
10:34

A High-content Assay for Monitoring AMPA Receptor Trafficking

Published on: January 28, 2019

8.1K

Roles for Arc in metabotropic glutamate receptor-dependent LTD and synapse elimination: Implications in health and

Julia R Wilkerson1, Joseph P Albanesi2, Kimberly M Huber1

  • 1Departments of Neuroscience, University of Texas Southwestern Medical Center, Dallas, TX 75390, United States.

Seminars in Cell & Developmental Biology
|October 4, 2017
PubMed

Insights

The Arc gene’s role in synaptic plasticity, specifically in long-term depression (LTD) and synapse elimination, is crucial for forming neural representations of learned experiences. Its dysregulation is linked to cognitive disorders.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Synaptic Plasticity

Background:

  • The Arc gene is transcribed in neural ensembles following experience-driven activity.
  • Arc mRNA is transported to dendrites for local translation, triggered by metabotropic glutamate receptors (mGluR1/5).

Purpose of the Study:

  • To review the mechanisms and functions of Arc in mGluR-induced long-term synaptic depression (mGluR-LTD) and synapse elimination.
  • To propose roles for Arc in experience-dependent neural plasticity and memory formation.
  • To discuss the link between Arc dysregulation and cognitive disorders.

Main Methods:

  • Review of existing literature on Arc gene function, synaptic plasticity, and mGluR signaling.
  • Analysis of mechanisms underlying experience-induced Arc transcription and translation.
  • Examination of Arc's role in AMPA receptor endocytosis and synaptic weakening.

Main Results:

  • mGluR-induced Arc synthesis mediates the weakening/elimination of excitatory synapses via AMPA receptor endocytosis in hippocampal and cerebellar neurons.
  • Experience-induced Arc mRNA primes CA1 neurons for mGluR-LTD.
  • Arc-dependent plasticity contributes to the formation of sparse neural representations.

Conclusions:

  • Arc plays a critical role in synaptic plasticity, including mGluR-LTD and synapse elimination.
  • These forms of plasticity are essential for encoding learned experiences into neural representations.
  • Aberrant Arc function and mGluR-LTD are implicated in intellectual disability, autism, and Alzheimer's disease.
Keywords:
Arc/Arg3.1DynaminLong-term synaptic depressionSynapse eliminationmGluR5

More Related Videos

BS3 Chemical Crosslinking Assay: Evaluating the Effect of Chronic Stress on Cell Surface GABAA Receptor Presentation in the Rodent Brain05:17

BS3 Chemical Crosslinking Assay: Evaluating the Effect of Chronic Stress on Cell Surface GABAA Receptor Presentation in the Rodent Brain

Published on: May 26, 2023

1.7K
Single Synapse Indicators of Glutamate Release and Uptake in Acute Brain Slices from Normal and Huntington Mice08:27

Single Synapse Indicators of Glutamate Release and Uptake in Acute Brain Slices from Normal and Huntington Mice

Published on: March 11, 2020

6.7K

Related Concept Videos

Long-term Depression01:03

Long-term Depression

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.
Calcium Ion Concentration Mechanism
If over...
3.4K
Long-term Depression01:05

Long-term Depression

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.
33.4K
Ligand-Gated Ion Channel Receptor: Gating Mechanism01:30

Ligand-Gated Ion Channel Receptor: Gating Mechanism

Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...
4.3K
Ligand-gated Ion Channels01:19

Ligand-gated Ion Channels

Ligand-gated ion channels are transmembrane proteins with a channel for ions to pass through and a binding site for a ligand. The channel opens only when a ligand attaches to the binding site.
Three Subfamilies of Ligand-gated Ion Channels
Ligand-gated ion channels fall into three subfamilies. The 'Cys-loop' includes the nicotinic acetylcholine receptors, γ-aminobutyric acid (GABA), glycine, and 5-hydroxytryptamine receptors. The second one is the 'Pore-loop' channels that...
14.5K
Long-term Potentiation01:25

Long-term Potentiation

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
LTP can occur when...
3.7K
Long-term Potentiation01:35

Long-term Potentiation

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.
58.9K