Abstract
The extraordinary ability of turtle brain to survive anoxia has created interest in defining its protective strategies for reasons which include: a) to increase understanding of anaerobiosis; b) to define factors underlying mammalian brain vulnerability; and c) to examine potential applications of these strategies to cerebrovascular and metabolic diseases. A key to turtle brain survival during anoxia is continued cation transport for prolonged periods and avoidance of anoxic depolarization. When inspiration of oxygen was halted under experimental conditions, many mechanisms of compensation became apparent in turtle brain that supported the maintenance of ion homeostasis. Brain blood flow was continued or increased, and oxygen and creatine phosphate (PCr) stores offered some immediate protection. As PCr declined, turtle brain became increasingly reliant upon anaerobic glycolysis. In fact, transmembrane ion gradients were lost during ischemia or during anoxia with glycolytic inhibition (superfusion of brain with iodoacetate) and, in contrast to anoxia, these latter insults soon became irreversible. Evoked potential activity was inhibited by anoxia suggesting that excitability (synaptic transmission) had declined with what is likely a compensatory lowering of energy consumption. Also, stimulus-provoked increases in Ko+ were cleared less rapidly. Ko+ recovery rates were most retarded at low Ko+ values suggesting that high Ko+ “loads” either overcame the apparent compensatory decrease in Ko+ clearance rates or that an additional transport mechanism was activated to promote rapid Ko+ reaccumulation when stimulus-provoked Ko+ increments were high. This secondary process may not be present in mammalian brain and it may protect turtle brain against anoxic depolarization.