Related Experiment Video

Updated: May 16, 2026

Mechanical Stimulation-induced Calcium Wave Propagation in Cell Monolayers: The Example of Bovine Corneal Endothelial Cells
10:46

Mechanical Stimulation-induced Calcium Wave Propagation in Cell Monolayers: The Example of Bovine Corneal Endothelial Cells

Published on: July 16, 2013

A key role for connexin hemichannels in spreading ischemic brain injury

Joanne O Davidson1, Colin R Green, Laura Bennet

  • 1Department of Physiology, The University of Auckland, Auckland, New Zealand.

Current Drug Targets
|November 23, 2012
PubMed

Insights

Cerebral ischemia causes brain damage, with secondary mitochondrial failure spreading injury. Suppressing connexin hemichannels may reduce this damage spread after brain insults.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Pathology

Background:

  • Cerebral ischemia, including stroke and hypoxia-ischemia (HI), causes significant brain damage across all ages.
  • HI injury in newborns and ischemic stroke in adults are major health concerns, leading to death and disability.
  • A delayed, secondary mitochondrial failure spreads HI injury, causing seizures and edema.

Purpose of the Study:

  • To investigate the role of connexin hemichannels in the spread of secondary mitochondrial failure after cerebral ischemia.
  • To explore the potential of targeting connexin hemichannels to mitigate brain damage progression.

Main Methods:

  • Review of existing evidence on connexin hemichannel function in neural insults.
  • Analysis of proposed mechanisms involving connexin hemichannels in spreading depression and cell death.
  • Examination of studies demonstrating the effects of connexin hemichannel suppression on injury spread.

Main Results:

  • Unopposed connexin hemichannels contribute to injury spread by releasing paracrine molecules (ATP, NAD+, glutamate) and mediating cell edema.
  • Connexin hemichannels facilitate cell-to-cell communication, propagating damage signals through a 'bystander effect'.
  • Evidence suggests connexin hemichannels are implicated in injury after various neural insults.

Conclusions:

  • Connexin hemichannels play a significant role in the secondary spread of brain damage following cerebral ischemia.
  • Suppressing connexin hemichannel activity or induction shows promise in reducing the extent of brain injury.
  • Targeting connexin hemichannels represents a potential therapeutic strategy for managing ischemic brain damage.

More Related Videos

A Preclinical Controlled Cortical Impact Model for Traumatic Hemorrhage Contusion and Neuroinflammation06:50

A Preclinical Controlled Cortical Impact Model for Traumatic Hemorrhage Contusion and Neuroinflammation

Published on: June 10, 2020

A Cell Culture Model for Studying the Role of Neuron-Glia Interactions in Ischemia11:36

A Cell Culture Model for Studying the Role of Neuron-Glia Interactions in Ischemia

Published on: November 14, 2020

Related Concept Videos

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...
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...
Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

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...
Ischemic Stroke l: Introduction01:15

Ischemic Stroke l: Introduction

Ischemic stroke is an acute cerebrovascular condition in which blood flow to a brain region is suddenly interrupted, leading to tissue infarction. Neurons depend on continuous oxygen and glucose supply, so even brief reductions in perfusion cause energy failure, ionic imbalance, and irreversible injury. Ischemic strokes are classified into thrombotic and embolic types based on their underlying mechanisms.Thrombotic MechanismsThrombotic stroke develops when a clot forms within a cerebral artery.
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
Secondary Spinal Cord Injury llI: Pathophysiology01:25

Secondary Spinal Cord Injury llI: Pathophysiology

Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...