[Ischemic and hypoxic depolarization in the rat neocortex].

Cortical negative DC potential shifts were studied on two experimental models: focal cortical ischemia provoked by a photothrombotic occlusion of the distal part of the middle cerebral artery (dMCA) and a combination of systemic hypoxia induced by bilateral ligation of the common carotid arteries (temporary ligation of the left artery and permanent ligation of the right one) with breathing with 0.5% carbon monoxide (CO). The perifocal ischemic depolarization (ID) after the dMCA thrombosis was found to reach 28-33 mV and then gradually decline during 80 min to a certain residual level about 5 mV. Spontaneous depolarization didn't occur during hypoxia but it was easily provoked in one or both hemispheres by the waves of the cortical spreading depression (SD). The amplitude of hypoxic depolarization (HD) didn't exceed 20 mV, was remarkably stable during hypoxic condition (more than 60 min) and returned to the baseline level within 20-30 min after the cessation of CO breathing and releasing of the left carotid artery. Despite the similar durations of the ID and HD, their functional consequences differed greatly. The ID led to a damage of the nervous tissue as evidenced by a reduction of the SD amplitude (to 20-25%) and biphasic change in persistent negative potential (PNP) evoked by the SD wave alone. The 1.5-2-fold increase in the PNP amplitude in the perifocal region was the most prominent outcome of the ID. In contrast to the ID, the SD and PNP characteristics were unchanged after the HD. Such a discrepancy between the ID and HD can be related with their different origin. The results suggest that the HD is produced by blood-brain barrier processes associated with the intensive vasospasm and vasogenic edema. Besides these phenomena, the other well-known factors such as a disturbance of permeability of neuronal membranes, glutamatemediated exitotoxicity, and tissue destruction determine the ID noxious influences.