Related Experiment Video

Updated: May 18, 2026

Acute Brain Trauma in Mice Followed By Longitudinal Two-photon Imaging
11:14

Acute Brain Trauma in Mice Followed By Longitudinal Two-photon Imaging

Published on: April 6, 2014

Blocking of connexin-mediated communication promotes neuroprotection during acute degeneration induced by mechanical

Vera Paschon1, Guilherme Shigueto Vilar Higa, Rodrigo Ribeiro Resende

  • 1Núcleo de Cognição e Sistemas Complexos, Centro de Matemática, Computação e Cognição, Universidade Federal do ABC, Santo André, São Paulo, Brazil.

Plos One
|October 3, 2012
PubMed

Insights

Connexin (Cx) channels in gap junctions (GJ) play a role in retinal neurodegeneration. Blocking Cx36 channels with quinine rapidly reduced cell death and apoptosis spread after mechanical trauma.

Area of Science:

  • Neuroscience
  • Ophthalmology
  • Cell Biology

Background:

  • Gap junctions (GJ) formed by connexins (Cx) are implicated in neurodegeneration, but their precise role remains debated.
  • Previous studies using knockout models yielded conflicting results regarding the neuroprotective effects of Cx-mediated coupling.
  • Retinal mechanical trauma provides a reproducible model to study neurodegeneration with defined spatial and temporal characteristics.

Purpose of the Study:

  • To investigate the role of connexin-mediated communication in retinal neurodegeneration following mechanical trauma.
  • To analyze the expression patterns of Cx36 and Cx43 during the neurodegenerative process.
  • To evaluate the therapeutic potential of modulating GJ channel activity for neuroprotection.

Main Methods:

  • Induction of focal mechanical retinal trauma in a reproducible animal model.
  • Analysis of Cx36 and Cx43 gene expression and protein distribution.
  • Assessment of cell death using lactate dehydrogenase (LDH) assays.
  • Pharmacological modulation of GJ channels using blockers (Carbenoxolone, Quinine) and openers.
  • Evaluation of apoptosis spread and caspase activity.

Main Results:

  • Cx36 and Cx43 exhibited distinct expression changes during retinal degeneration, with Cx36 localized near apoptotic cells.
  • Quinine, a Cx36-specific blocker, significantly reduced LDH release and apoptosis spread earlier than the broad-spectrum blocker CBX.
  • Quinine treatment downregulated key caspases involved in apoptotic pathways, unlike CBX treatment.

Conclusions:

  • Connexin channels and their specific subtypes, particularly Cx36, are actively involved in acute retinal neurodegeneration.
  • Targeting GJ channel permeability with specific blockers like quinine offers a promising strategy for rapid neuroprotection after retinal mechanical trauma.
  • Modulating GJ communication represents a potential therapeutic avenue for treating acute retinal injuries.

More Related Videos

Intravital Imaging of Axonal Interactions with Microglia and Macrophages in a Mouse Dorsal Column Crush Injury08:43

Intravital Imaging of Axonal Interactions with Microglia and Macrophages in a Mouse Dorsal Column Crush Injury

Published on: November 23, 2014

Related Concept Videos

Neurogenesis and Regeneration of Nervous Tissue01:15

Neurogenesis and Regeneration of Nervous Tissue

In the CNS, neurogenesis, the birth of new neurons from stem cells, is limited to the hippocampus in adults. In other regions of the brain and spinal cord, neurogenesis is almost non-existent due to inhibitory influences from neuroglia, especially oligodendrocytes, and the absence of growth-stimulating cues. The myelin produced by oligodendrocytes in the CNS inhibits neuronal regeneration. Furthermore, astrocytes proliferate rapidly after neuronal damage, forming scar tissue that physically...
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...
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...