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Related Concept Videos

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.
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 presynaptic neurons...
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 time, all...
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.
Calmodulin-dependent Signaling01:16

Calmodulin-dependent Signaling

Calmodulin (CaM) is a calcium-binding protein in eukaryotes that controls various calcium-regulated cellular processes. It has four calcium-binding sites that bind calcium to form the calcium-calmodulin ( Ca2+-CaM) complex. GPCR stimulation increases the calcium levels in the cells that bind to CaM and induces a conformational change.
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...
Role of Neurotransmitters in Memory01:23

Role of Neurotransmitters in Memory

Neurotransmitters are integral to the brain's communication system, enabling neurons to transmit signals across synapses. This chemical exchange underpins various cognitive functions, including memory processes. The role of neurotransmitters in memory is multifaceted, influencing the encoding, consolidation, and retrieval of memories through their action on different neural circuits.
 Glutamate and Synaptic Plasticity
Glutamate, the brain's main excitatory neurotransmitter, is critical for...

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Related Experiment Video

Updated: Jul 15, 2026

Investigation of Synaptic Tagging/Capture and Cross-capture using Acute Hippocampal Slices from Rodents
11:29

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Published on: September 4, 2015

eIF2alpha phosphorylation bidirectionally regulates the switch from short- to long-term synaptic plasticity and

Mauro Costa-Mattioli1, Delphine Gobert, Elad Stern

  • 1Department of Biochemistry and McGill Cancer Center, McGill University, Montreal, Quebec, Canada. mauro.costa-mattioli@mail.mcgill.ca

Cell
|April 10, 2007
PubMed
Summary

Altering eIF2alpha phosphorylation impacts memory and synaptic plasticity. Reduced phosphorylation enhances memory and late-long-term potentiation (L-LTP), while increased phosphorylation impairs them.

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Related Experiment Videos

Last Updated: Jul 15, 2026

Investigation of Synaptic Tagging/Capture and Cross-capture using Acute Hippocampal Slices from Rodents
11:29

Investigation of Synaptic Tagging/Capture and Cross-capture using Acute Hippocampal Slices from Rodents

Published on: September 4, 2015

Improved Preparation and Preservation of Hippocampal Mouse Slices for a Very Stable and Reproducible Recording of Long-term Potentiation
09:39

Improved Preparation and Preservation of Hippocampal Mouse Slices for a Very Stable and Reproducible Recording of Long-term Potentiation

Published on: June 26, 2013

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

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Synaptic Plasticity

Background:

  • Late-phase long-term potentiation (LTP) and long-term memory (LTM) depend on new gene expression.
  • The precise molecular mechanisms governing these processes remain incompletely understood.
  • Phosphorylation of eukaryotic initiation factor 2 alpha (eIF2alpha) globally inhibits translation but selectively boosts ATF4, a repressor of CREB-mediated late-LTP (L-LTP) and LTM.

Purpose of the Study:

  • To investigate the role of eIF2alpha phosphorylation in synaptic plasticity and behavioral learning.
  • To elucidate the regulatory function of eIF2alpha phosphorylation in L-LTP and LTM formation.

Main Methods:

  • Utilized a pharmacogenetic bidirectional approach in mice.
  • Examined the effects of reduced eIF2alpha phosphorylation in eIF2alpha(+/S51A) mice.
  • Investigated the impact of increased eIF2alpha phosphorylation using the small molecule Sal003 in the hippocampus.

Main Results:

  • Reduced eIF2alpha phosphorylation in eIF2alpha(+/S51A) mice lowered the threshold for L-LTP and enhanced memory.
  • Increased eIF2alpha phosphorylation via Sal003 injection resulted in only early-LTP and impaired LTM.
  • These findings implicate the eIF2alpha phosphorylation site as a critical regulator.

Conclusions:

  • eIF2alpha phosphorylation is a key molecular switch controlling L-LTP and LTM.
  • Modulating eIF2alpha phosphorylation offers a potential therapeutic target for memory disorders.
  • The balance of eIF2alpha phosphorylation is crucial for memory consolidation and synaptic plasticity.