Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Calmodulin-dependent Signaling

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 Memory

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...

Immunoglobulin-like Cell Adhesion Molecules

Immunoglobulin-like Cell Adhesion Molecules

Immunoglobulin-like cell adhesion molecules or Ig-CAMs are a versatile group of cell surface glycoproteins belonging to the immunoglobulin protein superfamily. Ig-CAMs possess the characteristic immunoglobulin protein domains and other domains such as the fibronectin type III domain. The Ig domains are glycosylated to varying degrees in different Ig-CAMs.
Ig-CAMs exhibit either homophilic binding (to other Ig-CAMs) or heterophilic binding (to other ligands such as integrins). While most Ig-CAMs...

Long-term Depression

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 Potentiation

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 Potentiation

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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Experience-dependent critical period for synaptic plasticity in the rat olfactory amygdala.

Frontiers in synaptic neuroscience·2026

Same author

Olfactory dysfunction and altered cortical excitability in the mouse model of Fragile X Syndrome.

Biological research·2025

Same author

Ketogenic diet administration later in life improves memory by modifying the synaptic cortical proteome via the PKA signaling pathway in aging mice.

Cell reports. Medicine·2024

Same author

Altered resting-state functional connectivity in hiPSCs-derived neuronal networks from schizophrenia patients.

Frontiers in cell and developmental biology·2022

Same author

Heterogeneous CaMKII-Dependent Synaptic Compensations in CA1 Pyramidal Neurons From Acute Hippocampal Slices.

Frontiers in cellular neuroscience·2022

Same author

Induced Pluripotent Stem Cell-Derived Neural Precursors Improve Memory, Synaptic and Pathological Abnormalities in a Mouse Model of Alzheimer's Disease.

Cells·2021

Search research articles

Related Experiment Video

Updated: May 14, 2026

Aversive Associative Learning and Memory Formation by Pairing Two Chemicals in Caenorhabditis elegans

Aversive Associative Learning and Memory Formation by Pairing Two Chemicals in Caenorhabditis elegans

Published on: June 23, 2022

The CaMKII/NMDAR complex as a molecular memory.

Magdalena Sanhueza¹, John Lisman

¹Department of Biology, Faculty of Sciences, University of Chile, Las Palmeras 3425, Santiago 7800024, Chile.

Molecular Brain

|February 16, 2013

Summary

This summary is machine-generated.

Calcium-calmodulin-dependent protein kinase II (CaMKII) activation by NMDA receptors (NMDARs) is crucial for memory stability. The CaMKII/NMDAR complex may act as a molecular tag, initiating a cascade for structural synaptic growth and stable memory storage.

More Related Videos

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

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

Published on: September 4, 2015

A High-throughput Calcium-flux Assay to Study NMDA-receptors with Sensitivity to Glycine/D-serine and Glutamate

A High-throughput Calcium-flux Assay to Study NMDA-receptors with Sensitivity to Glycine/D-serine and Glutamate

Published on: July 10, 2018

Related Experiment Videos

Last Updated: May 14, 2026

Aversive Associative Learning and Memory Formation by Pairing Two Chemicals in Caenorhabditis elegans

Aversive Associative Learning and Memory Formation by Pairing Two Chemicals in Caenorhabditis elegans

Published on: June 23, 2022

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

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

Published on: September 4, 2015

A High-throughput Calcium-flux Assay to Study NMDA-receptors with Sensitivity to Glycine/D-serine and Glutamate

A High-throughput Calcium-flux Assay to Study NMDA-receptors with Sensitivity to Glycine/D-serine and Glutamate

Published on: July 10, 2018

Area of Science:

Neuroscience
Molecular Biology
Synaptic Plasticity

Background:

Long-term potentiation (LTP) is a key mechanism for memory formation.
Calcium-calmodulin-dependent protein kinase II (CaMKII) activation by NMDA receptors (NMDARs) is essential for LTP induction.
The precise role of CaMKII in the maintenance of LTP and stable memory storage remains incompletely understood.

Purpose of the Study:

To evaluate the hypothesis that the CaMKII/NMDAR complex maintains LTP.
To elucidate the molecular mechanisms underlying structural synaptic growth in late LTP.
To propose a molecularly specific version of the tag/capture hypothesis for late LTP.

Main Methods:

Review of existing literature on LTP maintenance mechanisms.
Evaluation of evidence supporting the CaMKII/NMDAR complex hypothesis.
Integration of binding reactions to propose a molecular cascade for synaptic growth.

Main Results:

Substantial evidence supports the CaMKII/NMDAR complex's role in LTP maintenance.
The CaMKII/NMDAR complex is proposed to function as a molecular tag for late LTP.
A binding cascade involving densin, delta-catenin, and N-cadherin is suggested to mediate structural synaptic growth.

Conclusions:

The CaMKII/NMDAR complex is a strong candidate for LTP maintenance.
This complex initiates a cascade leading to increased AMPA channel content and synapse size.
Stable memory storage may involve the CaMKII/NMDAR complex and N-cadherin dimers, analogous to DNA base-pairing.