Extracellular pH and suppression of electrical activity during anoxia in turtle and rat brain

To evaluate the contribution of extracellular H⁺ activity toward depression of brain electrical activity during anoxia, extracellular pH (pH(e)) and field potentials were measured in turtle and rat olfactory bulbs with ion-selective microelectodes. This study tests the hypothesis that unique regulation of pH(e) contributes to the remarkable tolerance of turtle brain to prolonged anoxia. Hypercapnea (20% CO₂ ventilation) depressed olfactory bulb evoked potentials 25-30% in both rat and turtle. During anoxia, evoked potentials were completely abolished within 1 min in rat olfactory bulb but decreased to only 40% of control after 4 h in the turtle despite similar changes in brain pH(e). Anoxia-induced acidification of turtle brain was exacerbated by hypercapnea and was attenuated by hypocapnea or by hypocapnea plus intravenous infusion of sodium bicarbonate. However, these manipulations of pH(e) during anoxia in turtle brain had little effect on depression of evoked potentials. We conclude that energy failure, rather than extracellular acidification, is the major contributor toward suppression of electrical activity in mammalian brain and that preservation of energy balance, rather than unique pH regulation, is responsible for protection of turtle brain during anoxia.