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Related Concept Videos

The Blood-brain Barrier00:49

The Blood-brain Barrier

Overview
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...
Non-gated Ion Channels01:24

Non-gated Ion Channels

Ion channels are specialized proteins on the plasma membrane that allow charged ions to pass down their electrochemical gradient. Their main function is to maintain the membrane potential which is critical for cell viability. These channels are either gated or non-gated and can transport more than a thousand ions within milliseconds for the cellular event to occur.
Compared to the gated ion channels, the non-gated channels, also known as leakage or passive channels, have no gating mechanism.
Ligand-gated Ion Channels01:19

Ligand-gated Ion Channels

Ligand-gated ion channels are transmembrane proteins with a channel for ions to pass through and a binding site for a ligand. The channel opens only when a ligand attaches to the binding site.
Three Subfamilies of Ligand-gated Ion Channels
Ligand-gated ion channels fall into three subfamilies. The 'Cys-loop' includes the nicotinic acetylcholine receptors, γ-aminobutyric acid (GABA), glycine, and 5-hydroxytryptamine receptors. The second one is the 'Pore-loop' channels that include the...
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...
Ligand-gated Ion Channels01:19

Ligand-gated Ion Channels

Ligand-gated ion channels are transmembrane proteins with a channel for ions to pass through and a binding site for a ligand. The channel opens only when a ligand attaches to the binding site.
Three Subfamilies of Ligand-gated Ion Channels
Ligand-gated ion channels fall into three subfamilies. The 'Cys-loop' includes the nicotinic acetylcholine receptors, γ-aminobutyric acid (GABA), glycine, and 5-hydroxytryptamine receptors. The second one is the 'Pore-loop' channels that include the...

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Related Experiment Video

Updated: Jul 11, 2026

A Human Blood-Brain Interface Model to Study Barrier Crossings by Pathogens or Medicines and Their Interactions with the Brain
07:52

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Published on: April 9, 2019

Ischemia opens neuronal gap junction hemichannels.

Roger J Thompson1, Ning Zhou, Brian A MacVicar

  • 1Department of Psychiatry and Brain Research Centre, University of British Columbia, Vancouver, British Columbia V6T 2B5, Canada.

Science (New York, N.Y.)
|May 13, 2006
PubMed
Summary
This summary is machine-generated.

Stroke-induced neuronal damage involves large-conductance channels. Our study reveals that oxygen/glucose deprivation opens neuronal hemichannels, contributing to cell death during ischemic events.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Pathophysiology

Background:

  • Neuronal excitotoxicity is a key mechanism in stroke pathology.
  • This excitotoxicity is linked to the activation of poorly understood large-conductance ion channels.
  • Channel activation leads to neuronal swelling and disrupted calcium homeostasis.

Purpose of the Study:

  • To identify the specific channels involved in neuronal excitotoxicity during ischemic conditions.
  • To investigate the role of hemichannels in neuronal damage following oxygen and glucose deprivation (OGD).

Main Methods:

  • Induction of ischemic-like conditions using oxygen/glucose deprivation (OGD) in neurons.
  • Measurement of membrane currents and flux of small fluorescent molecules to detect hemichannel activity.
  • Application of hemichannel inhibitors to assess their effect on OGD-induced currents and dye flux.
  • Single-channel recordings to characterize hemichannel conductance.

Main Results:

  • Ischemic-like conditions (OGD) induced the opening of neuronal hemichannels.
  • Hemichannel opening was evidenced by large linear currents and the flux of fluorescent dyes across the neuronal membrane.
  • Single-channel recordings identified hemichannel openings with a conductance of 530 picosiemens.
  • Inhibitors of hemichannels effectively blocked both the observed current and dye flux.

Conclusions:

  • Hemichannel opening is a significant contributor to ionic dysregulation in neurons during stroke.
  • These findings suggest that hemichannels are a ubiquitous component of ischemic neuronal death.
  • Targeting hemichannel activity may offer a novel therapeutic strategy for stroke treatment.