X-Message-Number: 14441
Date: Sun, 10 Sep 2000 22:01:03 -0700 (PDT)
From: Doug Skrecky <>
Subject: glycolysis prevents anoxia damage

Title
  Glycolysis prevents
  anoxia-induced synaptic transmission damage in rat
  hippocampal slices.
Source
  Journal of Neurophysiology.  83(4):1830-9, 2000 Apr.
Abstract
  Prolonged anoxia can cause permanent damage to synaptic
  transmission in the mammalian CNS. We tested the hypothesis that lack of
  glucose is the major cause of irreversible anoxic transmission damage, and
  that anoxic synaptic transmission damage could be prevented by
  glycolysis in rat hippocampal slices. The evoked population
  spike (PS) was extracellularly recorded in the CA1 pyramidal cell layer after
  stimulation of the Schaffer collaterals. When the slice was superfused with
  artificial cerebrospinal fluid (ACSF) containing 4 mM glucose, following 10
  min anoxia, the evoked PS did not recover at all after 60
  min reoxygenation. When superfusion ACSF contained 10 mM glucose with or
  without 0.5 mM alpha-cyano-4-hydroxycinnate (4-CIN), after 60 min
  reoxygenation the evoked PS completely recovered following 10 min
  anoxia. When superfusion ACSF contained 20 mM glucose with
  or without 1 mM sodium cyanide (NaCN), after 60 min reoxygenation the evoked
  PS completely recovered even following 120 min anoxia. In
  contrast, when superfusion ACSF contained 4 mM glucose, following 10 min 1 mM
  NaCN chemical anoxia alone, without anoxic
  anoxia, the evoked PS displayed no recovery after 60 min
  reoxygenation. Moreover, when 16 mM mannitol and 16 sodium L-lactate were
  added into 4 mM glucose ACSF, following 10 min anoxia the
  evoked PS failed to recover at all after 60 min reoxygenation. The results
  indicate that elevated glucose concentration powerfully protected the
  synaptic transmission against anoxic damage, and the powerful protection is
  due to anaerobic metabolism of glucose and not a result of the higher
  osmolality in higher glucose ACSF. We conclude that lack of glucose is the
  major cause of anoxia-induced synaptic transmission damage,
  and that if sufficient glucose is supplied, glycolysis could
  prevent this damage in vitro.

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