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Related Concept Videos

Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

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An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
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Transient Ischemic Attack l: Introduction01:26

Transient Ischemic Attack l: Introduction

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A transient ischemic attack (TIA) is a brief episode of neurological dysfunction caused by a temporary, focal reduction in cerebral blood flow. Although symptoms resemble those of an ischemic stroke, the interruption in perfusion is short-lived and does not cause permanent infarction. TIAs are clinically important because they often serve as early warning events for future stroke.Mechanisms of Transient Cerebral IschemiaTransient cerebral ischemia may arise through several mechanisms. One...
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Ischemic Heart Disease: Overview01:17

Ischemic Heart Disease: Overview

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Ischemic heart disease occurs when the heart's blood supply dwindles, causing an ominous lack of oxygen and nutrients. This deficiency, stemming from reduced or obstructed blood flow, spells danger, leading to heart muscle damage and dysfunction.
Atherosclerosis, the primary malefactor, orchestrates this dangerous condition. It manifests as the accumulation of fatty deposits, akin to insidious plaques, within arterial walls. As time elapses, these plaques metamorphose, hardening and...
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Gap Junctions

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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...
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Gap Junctions01:27

Gap Junctions

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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...
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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.
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Related Experiment Video

Updated: Apr 21, 2026

Mechanical Stimulation-induced Calcium Wave Propagation in Cell Monolayers: The Example of Bovine Corneal Endothelial Cells
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Pannexin channels and ischaemia.

Roger J Thompson1

  • 1Department of Cell Biology and Anatomy, Hotchkiss Brain Institute, University of Calgary, Calgary, AB, T2N 4N1, Canada.

The Journal of Physiology
|November 12, 2014
PubMed
Summary

Ischaemic stroke involves brain blood flow loss. Targeting the pannexin-1 (Panx1) channel, activated by N-methyl-d-aspartate receptors (NMDARs) and Src kinases, may reduce neuronal death.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Ischemic Stroke Research

Background:

  • Ischaemic stroke results from disrupted brain blood flow, causing oxygen and glucose deprivation (OGD) and excitotoxicity.
  • N-methyl-d-aspartate receptors (NMDARs) play a key role in the excitotoxic cascade during ischaemia.
  • The ion channel pannexin-1 (Panx1) is a critical target influenced by NMDARs during ischaemic events.

Purpose of the Study:

  • To investigate the mechanism of Panx1 channel activation by NMDARs in the context of ischaemia.
  • To explore the role of Src family kinases in NMDAR-mediated Panx1 activation.
  • To evaluate the therapeutic potential of targeting Panx1 activation for reducing ischaemic brain injury.

Main Methods:

  • Experiments utilized hippocampal brain slices to study cellular mechanisms.

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  • NMDAR activation and its downstream effects on Panx1 were investigated.
  • The involvement of Src family kinases in Panx1 regulation was examined.
  • An interfering peptide targeting Panx1 (amino acids 305-318) was used to antagonize Panx1 opening.

    • Main Results:

    • Panx1 channels are activated by NMDARs via Src family kinases in hippocampal slices.
    • The precise interaction between Src kinases and Panx1 (phosphorylation vs. allosteric) remains under investigation.
    • An interfering peptide targeting Panx1 (aa 305-318) effectively antagonized Panx1 opening during simulated ischaemia and NMDAR over-activation.

    Conclusions:

    • NMDARs and Src kinases mediate the activation of Panx1 channels during ischaemia.
    • Targeting Panx1 activation presents a promising therapeutic strategy to mitigate neuronal damage in ischaemic stroke.
    • Inhibiting Panx1 opening could reduce anoxic depolarizations and subsequent neuronal death.