Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

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...
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.
Chemical Synapses01:26

Chemical Synapses

Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...

You might also read

Related Articles

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

Sort by
Same author

Upregulation of endocannabinoid signaling in vivo restores striatal synaptic plasticity and motor performance in Huntington's disease mice.

Journal of Huntington's disease·2025
Same author

Home cage-based insights into motor learning and strategy adaptation in a Huntington disease mouse model.

PloS one·2025
Same author

Synaptic modulation of glutamate in striatum of the YAC128 mouse model of Huntington disease.

Neurobiology of disease·2024
Same author

Deep behavioural phenotyping of the Q175 Huntington disease mouse model: effects of age, sex, and weight.

BMC biology·2024
Same author

Mechanisms of synapse-to-nucleus calcium signalling in striatal neurons and impairments in Huntington's disease.

Journal of neurochemistry·2024
Same author

Activin A targets extrasynaptic NMDA receptors to ameliorate neuronal and behavioral deficits in a mouse model of Huntington disease.

Neurobiology of disease·2023
Same journal

Reflections from Mathias Bähr, PhD, Editor-in-Chief for Molecular and Cellular Neuroscience, 2017-2026.

Molecular and cellular neurosciences·2026
Same journal

Advancing molecular and cellular neuroscience: Vision and priorities from the new editor-in-chief.

Molecular and cellular neurosciences·2026
Same journal

Apolipoprotein E in Alzheimer's disease: A review of APOE receptors, signalling pathways and therapeutic opportunities.

Molecular and cellular neurosciences·2026
Same journal

Inadvertent p75NTR signaling might cause inconsistencies in the neuroprotection offered by mesenchymal stem cells.

Molecular and cellular neurosciences·2026
Same journal

Corrigendum to "Depressed mitochondrial function and electron transport Complex II-mediated H2O2 production in the cortex of type 1 diabetic rodents" [Mol. Cell. Neurosci. Volume 90, July 2018, Pages 49-59].

Molecular and cellular neurosciences·2026
Same journal

Sleep deprivation and hippocampal integrity: Oxidative stress mediated neuronal, memory and behavioral alterations and the restorative role of sleep recovery.

Molecular and cellular neurosciences·2026
See all related articles

Related Experiment Video

Updated: Jun 1, 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

Mechanisms underlying NMDA receptor synaptic/extrasynaptic distribution and function.

Clare M Gladding1, Lynn A Raymond

  • 1Department of Psychiatry, University of British Columbia, Vancouver, BC, Canada. clareg@interchange.ubc.ca

Molecular and Cellular Neurosciences
|May 24, 2011
PubMed
Summary
This summary is machine-generated.

The N-methyl-D-aspartate receptor (NMDAR) is vital for brain function. Its location impacts function, and mislocalization contributes to neurological diseases, suggesting new therapeutic targets.

More Related Videos

A High-throughput Calcium-flux Assay to Study NMDA-receptors with Sensitivity to Glycine/D-serine and Glutamate
04:48

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

Published on: July 10, 2018

3D Modeling of Dendritic Spines with Synaptic Plasticity
07:13

3D Modeling of Dendritic Spines with Synaptic Plasticity

Published on: May 18, 2020

Related Experiment Videos

Last Updated: Jun 1, 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

A High-throughput Calcium-flux Assay to Study NMDA-receptors with Sensitivity to Glycine/D-serine and Glutamate
04:48

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

Published on: July 10, 2018

3D Modeling of Dendritic Spines with Synaptic Plasticity
07:13

3D Modeling of Dendritic Spines with Synaptic Plasticity

Published on: May 18, 2020

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cell Biology

Background:

  • The N-methyl-D-aspartate receptor (NMDAR) plays a critical role in synaptic neurotransmission, neuronal development, and learning and memory.
  • NMDARs traffic between synaptic and extrasynaptic sites, with location significantly influencing their physiological function.
  • Mechanisms regulating NMDAR localization and function, including post-translational modifications and protein interactions, can differ based on receptor location.

Purpose of the Study:

  • To review the molecular mechanisms governing NMDAR localization.
  • To explore how these mechanisms operate in both physiological and pathological conditions.
  • To highlight the significance of NMDAR mislocalization in neurological disorders.

Main Methods:

  • Literature review of recent studies on NMDAR function and regulation.
  • Analysis of molecular mechanisms controlling NMDAR trafficking and subcellular localization.
  • Examination of the role of NMDAR mislocalization in disease pathogenesis.

Main Results:

  • NMDARs exhibit dynamic trafficking between synaptic and extrasynaptic locations.
  • Specific molecular mechanisms regulate NMDAR localization and function differently at distinct cellular sites.
  • NMDAR mislocalization is implicated as a key factor in the dysfunction observed in neurological conditions like Alzheimer's disease and ischemia.

Conclusions:

  • Understanding NMDAR localization is crucial for comprehending glutamatergic function.
  • NMDAR mislocalization is a significant contributor to neurological disease pathology.
  • Targeting NMDAR mislocalization and downstream signaling pathways offers potential therapeutic strategies for NMDAR-related disorders.