Effects of anoxia and recovery on the neurotransmission and level of high-energy phosphates in thin hippocampal slices from the guinea-pig

Abstract

The effects of anoxia and recovery on the neuronal transmission and the levels of high-energy phosphates such as ATP and phosphocreatine were studied using thin hippocampal slices from the guineapig. For the index of neuronal activity, postsynaptic field potentials were recorded in the CA3 and CA4 regions after electrical stimulation to the dentate gyrus during deprivation of oxygen and glucose from the perfusion medium at 36.5°C. With deprivation of both oxygen and glucose from the medium, neuronal activity was abolished in 6–8 min. When the deprivation period was extended longer than 15 min, no recovery in the postsynaptic field potentials was observed. The concentrations of ATP and phosphocreatine in the slices decreased to 30–40% of original levels after 10 min deprivation of oxygen and glucose. ATP and phosphocreatine recovered to the original levels with the readmission of oxygen and glucose after 10 min anoxia, but the recovery of the ATP was worsened by the longer period of deprivation. Deprivation of oxygen only slowly decreased the amplitude of postsynaptic field potentials and blocked the neuronal activity after 70 min deprivation. The postsynaptic field potentials did not reappear after 180 min deprivation of oxygen. Even 120 min after deprivation of oxygen, the ATP and phosphocreatine levels were maintained at 60–70% of originals, whereas they both decreased to 30% after 150 min anoxia. The recovery of ATP even after 150 min anoxia was 64% and the recovery of phosphocreatine was over 100% even after 180 min anoxia. The survival times, the period of anoxia after which the neuronal function was able to recover, were 10 min in the case of oxygen and glucose deprivation and 150 min in the case of deprivation of oxygen only. Thus the presence of glucose was critical for the preservation of neuronal tissue during anoxia.