The Journal of Neurophysiology Vol. 88 No. 1 July 2002, pp. 236-248
Copyright ©2002 by the American Physiological Society
Protective Effect of High Glucose Against Ischemia-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 Department of Anaesthesia, St. Michael's Hospital,
University of Toronto, Toronto, Ontario M5B 1W8 Canada
Tian, Guo-Feng and
Andrew J. Baker.
Protective Effect of High Glucose Against Ischemia-Induced
Synaptic Transmission Damage in Rat Hippocampal Slices. J. Neurophysiol. 88: 236-248, 2002. Cerebral ischemic damage is an important cause of morbidity and
mortality. However, there is conflicting evidence regarding the effect
of the extracellular glucose concentration in focal and global ischemic
injury. This study was designed to investigate this effect in
ischemia-induced synaptic transmission damage in rat hippocampal
slices. Slices were superfused with artificial cerebrospinal fluid
(ACSF) containing various concentrations of glucose before and after
ischemia. The evoked somatic postsynaptic population spike (PS) and
dendritic field excitatory postsynaptic potential (fEPSP) were
extracellularly recorded in the CA1 stratum pyramidal cell layer and s.
radiatum after stimulation of the Schaeffer collaterals, respectively.
The glucose concentration in ACSF before and after ischemia determined
the duration of ischemia tolerated by synaptic transmission as
demonstrated by complete recovery of the somatic PS and dendritic
fEPSP. Specifically, the somatic PS and dendritic fEPSP completely
recovered following 3, 4, and 5 min of ischemia only when slices were
superfused with ACSF containing 4, 10, and 20 mM glucose before and
after ischemia, respectively. The latencies of the somatic and
dendritic ischemic depolarization (ID) occurrence in the CA1 s.
pyramidal cell layer and s. radiatum were significantly longer with 10 than 4 mM glucose in ACSF before ischemia and significantly longer with
20 than 10 mM glucose in ACSF before ischemia. Regardless of the
glucose concentration in ACSF before and after ischemia, the somatic PS and dendritic fEPSP only partially recovered when ischemia was terminated at the occurrence of ID. These results indicate that high
glucose in ACSF during the period before and after ischemia significantly protects CA1 synaptic transmission against in vitro ischemia-induced damage through postponing the occurrence of ID.
