X-Message-Number: 14988
From: 
Date: Tue, 21 Nov 2000 21:43:49 EST
Subject: glucose and hippocampal anoxia

 Following is an edited and abridged version of an interesting abstract:

 J Neurophysiol 83: 1830-1839. 

Glycolysis Prevents Anoxia-Induced Synaptic Transmission Damage in Rat 
Hippocampal Slices 
Guo-Feng Tian and Andrew J. Baker 
Traumatic Brain Injury Laboratory, Cara Phelan Centre for Trauma Research and 
the Department of Anaesthesia, St. Michael's Hospital, University of Toronto, 
Toronto, Ontario M5B 1W8, Canada 


 Prolonged anoxia can cause permanent damage to synaptic transmission in the 
mammalian CNS [Central Nervous System]. 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. When the slice was superfused with artificial 
cerebrospinal fluid (ACSF) containing 4 mM glucose, following 10 min anoxia, 
the evoked PS [population spike] did not recover at all after 60 min 
reoxygenation. When superfusion ACSF contained 10 mM glucose with or without 
0.5 mM -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 [chemically induced] alone, without anoxic 
anoxia [induced by lack of oxygen], 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.

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