Voltage-gated sodium channel Nav1.5 contributes to astrogliosis in an in vitro model of glial injury via reverse Na+/Ca2+ exchange

This study investigates how brain cells called astrocytes react to injury. Astrocytes change after brain or spinal cord damage, a process called astrogliosis. The researchers focused on voltage-gated sodium channels, specifically Nav1.5, and their role in this process. The experiments involved creating a scratch injury on a layer of astrocytes grown in the lab. The scientists then observed how the cells responded, particularly looking at cell movement (migration) and multiplication (proliferation). The researchers found that blocking Nav1.5, a specific type of sodium channel, reduced the astrocytes' ability to move and multiply to heal the scratch. This suggests that Nav1.5 plays a key role in how astrocytes respond to injury.

• 1
  Pharmacological treatment with TTX and KB-R7943, and knockdown of Nav1.5 mRNA attenuates wound closure after mechanical injury, involving both migration and proliferation.
• 2
  Astrocytes display a robust [Ca2+]i transient after mechanical injury, and TTX, KB-R7943, and Nav1.5 mRNA knockdown attenuates this [Ca2+]i response.
• 3
  VGSC activity, in particular, by way of alterations in [Ca2+]i, has link between the activity of VGSCs and astrogliosis.