Protective effect of high glucose against ischemia-induced synaptic transmission damage in rat hippocampal slices.
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.
Tian
Guo-Feng
GF
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. fiang@smh.toronto.on.ca
Baker
Andrew J
AJ
D000818:Animals; D002545:Brain Ischemia / Q000503:physiopathology*; D004305:Dose-Response Relationship, Drug; D004558:Electric Stimulation; D004594:Electrophysiology; D005071:Evoked Potentials; D005947:Glucose / Q000008:administration & dosage* / Q000494:pharmacology; D006624:Hippocampus / Q000098:blood supply*; D066298:In Vitro Techniques; D008297:Male; D018696:Neuroprotective Agents / Q000008:administration & dosage* / Q000494:pharmacology; D009994:Osmolar Concentration; D051381:Rats; D017207:Rats, Sprague-Dawley; D011930:Reaction Time / Q000187:drug effects; D009435:Synaptic Transmission / Q000187:drug effects*
D018696:Neuroprotective Agents; D005947:Glucose