Hippocampal slices exposed to brief
anoxia combined with elevated
glucose exhibit greater postanoxic recovery of synaptic transmission.
Glucose may have improved recovery of synaptic transmission by enhancing the production of metabolic energy during and after
anoxia. This enhancement should provide more
ATP for energy-requiring ion transport processes, and lead (1) to a delayed onset of complete depolarization of CA1 pyramidal cells during
anoxia (anoxic depolarization) and (2) to greater ion transport activity following
anoxia. A delay in anoxic depolarization would protect neurons from damage if the duration of anoxic depolarization was shortened. Greater postanoxic ion transport would allow the re-establishment of ion gradients supportive of neuronal and synaptic excitability. The effects of
glucose and
anoxia on ion homeostasis and synaptic transmission were examined in rat hippocampal slices exposed to different
glucose concentrations (5-20 mM). The duration of anoxic depolarization was held constant so that postanoxic damage related to this duration was controlled. We found that K+ transport and recovery of synaptic transmission after
anoxia in hippocampal slices improved as
glucose concentration increased. Also, anoxic depolarization was delayed as
glucose concentration increased. Thus, added
glucose may improve postanoxic recovery of synaptic transmission by better supporting ion transport.