https://opaganibinhibitor.com/....subacute-pain-trajec
We identified pharmacologically and genetically current as being mediated by Kir2.1 ion stations whose expression at the cellular membrane is increased 2 days after SNI. The inhibition of Kir2.1 with ML133 and siRNA reversed the RMP hyperpolarization and highly reduced the currents of microglial cells 2 times after SNI. These electrophysiological modifications occurred coincidentally to the peak of microglial expansion following nerve injury. In vitro, ML133 drastically reduc
Respect!
Kommentar
Delen
