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Related Concept Videos

Long-term Potentiation01:25

Long-term Potentiation

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

Long-term Potentiation

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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.
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Related Experiment Video

Updated: Mar 2, 2026

A High-content Assay for Monitoring AMPA Receptor Trafficking
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The Activity-Induced Long Non-Coding RNA Meg3 Modulates AMPA Receptor Surface Expression in Primary Cortical Neurons.

Men C Tan1,2, Jocelyn Widagdo1,2, Yu Q Chau1,2

  • 1Clem Jones Centre for Ageing Dementia Research, The University of QueenslandBrisbane, QLD, Australia.

Frontiers in Cellular Neuroscience
|May 19, 2017
PubMed
Summary
This summary is machine-generated.

Long non-coding RNA Meg3 plays a key role in synaptic plasticity by regulating AMPA receptor trafficking. This discovery sheds light on the molecular mechanisms underlying learning and memory.

Keywords:
AMPA receptorsLTPPTEN/PI3K/AKTepigeneticslong non-coding RNAmaternally expressed gene 3 (Meg3)receptor traffickingsynaptic potentiation

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • RNA transcription is vital for synaptic plasticity, learning, and memory.
  • The role of long non-coding RNAs (lncRNAs) in long-term potentiation (LTP) remains largely unknown.
  • Specific lncRNA clusters in the imprinted Dlk1-Dio3 region are implicated in neuronal function.

Purpose of the Study:

  • To investigate the role of lncRNAs, specifically the Meg3 cluster, in synaptic plasticity.
  • To determine the expression patterns of Meg3, Rtl1-AS, Meg8, and Meg9 in neurons.
  • To elucidate the molecular mechanisms by which Meg3 influences LTP.

Main Methods:

  • Stimulation of primary cortical neurons with glycine and N-methyl-D-aspartate receptor (NMDAR) activation.
  • In vivo analysis in mouse hippocampus following cued fear conditioning.
  • Assessment of lncRNA localization (nucleus and cytoplasm).
  • Functional assays involving Meg3 loss-of-function and AMPA receptor subunit (GluA1) trafficking.
  • Analysis of the phosphatidylinoside-3-kinase (PI3K)/AKT and PTEN signaling pathways.

Main Results:

  • Expression of the Meg3 lncRNA cluster (Meg3, Rtl1-AS, Meg8, Meg9) was demonstrated in primary cortical neurons and mouse hippocampus.
  • Meg3 was found to be expressed in both the nucleus and cytoplasm.
  • Meg3 loss-of-function impaired glycine-induced GluA1 AMPA receptor trafficking to the plasma membrane, a key feature of LTP.
  • Aberrant AMPA receptor trafficking was linked to dysregulation of the PTEN/PI3K/AKT signaling pathway.

Conclusions:

  • This study provides the first evidence for a functional role of the lncRNA Meg3 in synaptic plasticity.
  • Meg3 is involved in regulating the PTEN/PI3K/AKT signaling cascade in neurons.
  • Meg3 influences LTP by modulating AMPA receptor trafficking, offering new insights into learning and memory mechanisms.