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

Gap Junctions01:37

Gap Junctions

Multicellular organisms employ a variety of ways for cells to communicate with each other. Gap junctions are specialized proteins that form pores between neighboring cells in animals, connecting the cytoplasm between the two, and allowing for the exchange of molecules and ions. They are found in a wide range of invertebrate and vertebrate species, mediate numerous functions including cell differentiation and development, and are associated with numerous human diseases, including cardiac and...
Gap Junctions01:27

Gap Junctions

The cytoplasm of adjacent animal cells can exchange small molecules, ions, and secondary messengers via the communication channels which form the gap junctions. These junctions comprise a few hundred to thousands of molecular channels, each made of two halves, called the connexon hemichannel. A connexon is a hexamer of six transmembrane connexin proteins, which assemble radially, thus forming a pore or channel in the center. One connexon hemichannel docks with a corresponding connexon on the...
Contact-dependent Signaling01:19

Contact-dependent Signaling

Contact-dependent signaling, as the name suggests, requires that communicating cells be in direct contact with each other. This is achieved either through receptor-ligand interactions or by specialized cytoplasmic channels that allow the flow of small molecules between cells. In animal cells, channels called gap junctions facilitate contact-dependent signaling in certain tissues, whereas, plasmodesmata perform a similar function in plants.
Gap Junctions
In animal cells, gap junctions are formed...
Overview of Synapses01:25

Overview of Synapses

A synapse is a specialized structure where two neurons connect, allowing them to pass an electrical or chemical signal to another neuron. It is the point of communication between neurons. The term "synapse" is derived from the Greek word "synapsis," which means "conjunction." The entire process of neural communication revolves around the synapse. When activated, a neuron releases chemicals known as neurotransmitters into the synapse. These neurotransmitters cross the synapse and bind to...
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...
Overview of Cell-Cell Junctions01:14

Overview of Cell-Cell Junctions

The complex three-dimensional arrangement of cells in any multicellular organism is defined and maintained by interactions of cells with each other and the extracellular matrix. Cell-cell junctions are specialized structures where the multi-protein complexes on one cell interact with the multi-protein complexes on another  cell. These cell junctions are classified  into three main types based on their function — occluding, anchoring, and gap junctions.
Occluding or Tight Junctions
Tight...

You might also read

Related Articles

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

Sort by
Same author

The many meanings of Alzheimer's disease and why they matter for policy, research, and care.

GeroScience·2026
Same author

MarkVCID2 Consortium for Clinical Validation of Biomarkers of Cerebral Small Vessel Disease: Validation Framework and Baseline Characteristics.

Annals of neurology·2025
Same author

The future of biomarkers for vascular contributions to cognitive impairment and dementia (VCID): proceedings of the 2025 annual workshop of the Albert research institute for white matter and cognition.

GeroScience·2025
Same author

Non-literacy biased, culturally fair cognitive detection tool in primary care patients with cognitive concerns: a randomized controlled trial.

Nature medicine·2024
Same author

Instrumental validation of free water, peak-width of skeletonized mean diffusivity, and white matter hyperintensities: MarkVCID neuroimaging kits.

Alzheimer's & dementia (Amsterdam, Netherlands)·2022
Same author

An introduction to therapeutic approaches to vascular cognitive impairment.

Cerebral circulation - cognition and behavior·2021

Related Experiment Video

Updated: Jul 11, 2026

Modeling Neuronal Death and Degeneration in Mouse Primary Cerebellar Granule Neurons
10:36

Modeling Neuronal Death and Degeneration in Mouse Primary Cerebellar Granule Neurons

Published on: November 6, 2017

Gap junctions are required for NMDA receptor dependent cell death in developing neurons.

Juan Carlos de Rivero Vaccari1, Roderick A Corriveau, Andrei B Belousov

  • 1Department of Cell Biology and Anatomy, Louisiana State University Health Sciences Center, New Orleans, USA.

Journal of Neurophysiology
|September 15, 2007
PubMed
Summary

Neuronal gap junctions are critical for N-methyl-D-aspartate (NMDA) receptor-regulated cell death during development. Blocking these junctions protects neurons from NMDA receptor dysfunction, suggesting a collaborative role in neuronal survival.

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

Examination of Anatomical Features of Retinal Ganglion Cells Under N-methyl-D-aspartic Acid (NMDA)-induced Excitotoxicity
07:11

Examination of Anatomical Features of Retinal Ganglion Cells Under N-methyl-D-aspartic Acid (NMDA)-induced Excitotoxicity

Published on: September 19, 2025

Related Experiment Videos

Last Updated: Jul 11, 2026

Modeling Neuronal Death and Degeneration in Mouse Primary Cerebellar Granule Neurons
10:36

Modeling Neuronal Death and Degeneration in Mouse Primary Cerebellar Granule Neurons

Published on: November 6, 2017

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

Examination of Anatomical Features of Retinal Ganglion Cells Under N-methyl-D-aspartic Acid (NMDA)-induced Excitotoxicity
07:11

Examination of Anatomical Features of Retinal Ganglion Cells Under N-methyl-D-aspartic Acid (NMDA)-induced Excitotoxicity

Published on: September 19, 2025

Area of Science:

  • Neuroscience
  • Cell Biology
  • Developmental Biology

Background:

  • N-methyl-D-aspartate (NMDA) receptors are implicated in neuronal survival and death during development, trauma, and ischemia.
  • Neuronal coupling via gap junctions is elevated during these critical conditions, but their role in NMDA receptor-mediated cell death remains unclear.

Purpose of the Study:

  • To investigate the role of neuronal gap junction coupling in NMDA receptor-regulated cell death in developing neurons.

Main Methods:

  • Utilized primary hypothalamic cultures to examine NMDA receptor function and gap junction coupling.
  • Employed pharmacological inactivation of gap junctions and genetic knockout of connexin 36.
  • Assessed neuronal cell death under conditions of NMDA receptor inactivation or hyperactivation, and varying gap junction coupling levels.

Main Results:

  • NMDA receptor inactivation or hyperactivation induced significant neuronal cell death in cultures with high developmental gap junction coupling.
  • Modulating NMDA receptor function when gap junction coupling was low had minimal impact on cell survival.
  • Inactivation of gap junctions or knockout of connexin 36 abolished NMDA receptor dysfunction-induced cell death.

Conclusions:

  • Neuronal gap junctions play a critical role in mediating cell death resulting from NMDA receptor hypofunction or hyperfunction in developing neurons.
  • Proposes a novel hypothesis that NMDA receptors and gap junctions function synergistically to regulate neuronal survival.