NEURON-GLIAL INTERACTION DURING INJURY AND EDEMA OF THE CNS

During injury and ischemia of the CNS mediator compounds are released or activated which cause secondary swelling and damage of nerve cells. Such mediators are glutamate, acidosis, free fatty acids, or high ext racellular potassium. Glial homeostatic mechanisms are activated to pr event the secondary injury from these mediators. The glial clearance m echanisms have been studied in detail using in vitro systems allowing for a close control of the glial environment. Current evidence suggest s glial swelling to occur together with glutamate uptake or in respons e to extracellular acidosis. Glial swelling, therefore, is rather the result of homeostatic mechanisms than an indication of glial demise.