Is neuroglia a protector of neurons?
Our results indicate that normal glial function is an obstacle for SD spread. In our previous report (Largo et al. 1996) we suggested that the selective impairment of glial function imitates the condition of ischemic penumbra. Astrocyte swelling is the earliest reaction after several brain insults such as stroke (Kimelberg et al. 1990). Among the similarities was the generation of SD waves initiated near the dialysis probe but spreading into adjacent tissue. Recurrent SD waves appeared to be instrumental in the demise of neurons in FC poisoning, as they are in the ischemic penumbra(Hossmann 1994; Largo et al. 1996). It is known that astrocytes survive hypoxia much better than neurons. The neuronal injury caused by FC is most likely secondary to the loss of some supporting function by glial cells. We envisage glial tissue as limiting the duration of depolarization and constraining the spread of SD triggered by ischemia or other insults and therefore contributing to neuron survival in a
