Anoxia and NMDA Receptors

  • K. Krnjević
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 268)


Brief periods of anoxia cause a marked, but apparently fully reversible interruption of integrated brain function, whose cellular mechanism is not yet fully understood. For some 50 years it has been known that the hippocampus is one of the first brain regions to be affected by anoxia (Sugar and Gerard 1937). This disruption results from at least two major changes: one is a marked enhancement of K+ conductance in pyramidal neurons, and a corresponding fall in excitability (Hansen et al. 1982; Misgeld and Frotscher 1984); another is sharp depression of Ca2+ currents (Krnjević and Leblond 1987; 1989). The latter may be of importance in explaining the block of synaptic transmission, as well as perhaps the early loss of cognitive function, in certain aspects of which hippocampal Ca2+ signals appears to play an essential role (eg. Teyler and DiScenna, 1987; Smith, 1987). A major component of the Ca2+ fluxes involved in long-term plastic changes follows activation of hippocampal NMDA receptors (Collingridge et al., 1983; McDermott et al., 1986); so it was of interest to see how anoxia and NMDA receptors might interact. This question could also be important in the light of much evidence that NMDA receptor-mediated Ca2+ influx is probably responsible for the selective necrosis of hippocampal pyramids (especially in CAl) induced by prolonged anoxia/ischemia (Choi, 1988; Siesjö and Bengtsson, 1989). This article briefly reviews some relevant experiments performed on hippocampal slices.


NMDA Receptor Hippocampal Slice Depolarize Effect Cytoplasmic Calcium Concentration Reversible Interruption 
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Copyright information

© Springer Science+Business Media New York 1990

Authors and Affiliations

  • K. Krnjević
    • 1
  1. 1.Anaesthesia Research DepartmentMcGill UniversityMontréalCanada

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