Acute neural damage in the rat neocortex in vitro induced by a combination of anoxia and mechanical stress.
To elucidate the mechanisms of neural damage after brain ischemia, rat neocortical slices were exposed to anoxia at room temperature for 1 h, and other slices were prepared from the neocortical blocks exposed to anoxia at room temperature for 1 h. Field potentials elicited by the stimulation of layer IV were recorded in supragranular layers in these slices. No clear damage was observed electrophysiologically or morphologically in these slices. In contrast, a complete loss of the trans-synaptic field potentials and a decrease in the density of the cells stained with Neutral Red were elicited by injecting an anoxic medium into the neocortical blocks at room temperature for 1 h. In the slice preparations, the injection of the anoxic medium failed to reproduce clear neural damage, while a combination of mechanical stress and anoxia elicited a complete loss of trans-synaptic potentials; this was alleviated by Gd3+ (50 microM) and D(-)-2-amino-5-phosphonovaleric acid (100 microM). These results indicate that a combination of mechanical stress and anoxia produces acute and severe neural damage even at room temperature in vitro. The mechanism of the damage and the relationship between the neural damage in vitro and in vivo are discussed.