Suppression of evoked potentials with continued ion transport during anoxia in turtle brain.

A key to turtle brain survival during anoxia is continued ion transport and avoidance of anoxic depolarization. Previous findings that ATP concentration remained constant during prolonged anoxia and calculations that ATP production decreased indicate that compensatory processes, other than consumption of energy stores or increased anaerobic glycolysis, must also contribute to ion homeostasis and brain survival. To determine whether preservation of ion transport is associated with changes in electrophysiology during loss of oxidative metabolism, the brains of pentobarbital sodium-anesthetized turtles were electrically stimulated 1) to provoke measurable increments in extracellular K+ activity (a degrees k) for determination of rates of K+ reaccumulation at the stimulus site and 2) to elicit polysynaptic extracellular field potentials (evoked potentials) recordable in the olfactory bulb. During anoxia, base-line a degrees k rose only a few millimolar, and rates of reaccumulation of K+, incremented by stimulation were slightly but not significantly slowed. In contrast, postsynaptic orthodromic responses of olfactory bulb granule cells were markedly depressed by anoxia. Monosynaptic responses of granule cells to antidromic stimulation of the lateral olfactory tract were less affected, and compound action potentials in the olfactory nerve were unchanged by anoxia. These data suggest that synaptic transmission in turtle brain, as in that of mammal, is highly dependent on oxidative metabolism and that the turtle brain may effectively conserve energy for ion transport during anoxia by depression of electrical activity.