First Responders to Hyperosmotic Stress in Murine Astrocytes: Connexin 43 Gap Junctions Are Subject to an Immediate Ultrastructural Reorganization.

In a short-term model of hyperosmotic stress, primary murine astrocytes were stimulated with a hyperosmolar sucrose solution for five minutes. Astrocytic gap junctions, which are mainly composed of Connexin (Cx) 43, displayed immediate ultrastructural changes, demonstrated by freeze-fracture replica immunogold labeling: their area, perimeter, and distance of intramembrane particles increased, whereas particle numbers per area decreased. Ultrastructural changes were, however, not accompanied by changes in Cx43 mRNA expression.

Oxygen-Glucose Deprivation in Mouse Astrocytes is Associated with Ultrastructural Changes in Connexin 43 Gap Junctions.

In the intact brain, astrocytes play an important role in a number of physiological functions like spatial buffering of potassium, maintenance of calcium homeostasis, neurotransmitter release, regulation of the cerebral blood flow, and many more. As pathophysiological events upon hypoxic-ischemic brain injury include excitotoxicity by glutamate release as well as oxidative stress, astrocytes and their gap junction-based syncytium are of major relevance for regulating the extent of resulting brain damage. The gap junction protein Connexin (Cx) 43 contributes mainly to the astrocytic intercellular communication.