Related Experiment Video
Updated: Feb 7, 2026

Recording Gap Junction Current from Xenopus Oocytes
Published on: January 21, 2022
Blockade of gap junctions in vivo provides neuroprotection after perinatal global ischemia
Mara H de Pina-Benabou1, Vanessa Szostak, Andreas Kyrozis
1Department of Cell Biology and Anatomy, New York Medical College, Valhalla, NY 10595, USA.
Background And Purpose:
We investigated the contribution of gap junctions to brain damage and delayed neuronal death produced by oxygen-glucose deprivation (OGD).
Methods:
Histopathology, molecular biology, and electrophysiological and fluorescence cell death assays in slice cultures after OGD and in developing rats after intrauterine hypoxia-ischemia (HI).
Results:
OGD persistently increased gap junction coupling and strongly activated the apoptosis marker caspase-3 in slice cultures. The gap junction blocker carbenoxolone applied to hippocampal slice cultures before, during, or 60 minutes after OGD markedly reduced delayed neuronal death. Administration of carbenoxolone to ischemic pups immediately after intrauterine HI prevented caspase-3 activation and dramatically reduced long-term neuronal damage.
Conclusions:
Gap junction blockade may be a useful therapeutic tool to minimize brain damage produced by perinatal and early postnatal HI.
Related Concept Videos
Gap Junctions
Neuromuscular Junction And Blockade
Gap Junctions
Global Climate Change
P-N junction
The Neuromuscular Junction

