BRIEF PERIODS OF ISCHEMIA IN HYPERGLYCEMIC RATS INDUCE HIPPOCAMPAL CA1 DAMAGE IN THE ABSENCE OF CELL-MEMBRANE DEPOLARIZATION AND CALCIUM INFLUX

The objective of the study was to explore whether neuronal injury incu rred as a result of brief periods of ischemia is aggravated by preisch emic hyperglycemia. Anesthetized rats were subjected to 2.5 min of isc hemia, and allowed 7 days of recirculation for histopathological evalu ation of CA1 hippocampus damage. Normo- and hyperglycemic animals had plasma glucose concentrations of 5 - 7 and, 18 - 20 mM, respectively. DC potentials shifts and extracellular calcium concentration (Ca-e(2+) ) were measured with microelectrodes. Both normo- and hyperglycemic an imals had an average of 100 - 150 necrotic CA1 neurons (about 10 - 15 % of control), with no difference between the groups. However, whereas cells in normoglycemic animals showed a DC potential shift of about 3 min duration, with uptake of virtually all extracellular calcium, cel ls in hyperglycemic ones did not depolarise, nor was there a decrease in Ca-e(2+). It is concluded that neither membrane depolarisation nor cellular uptake of calcium is required to trigger ischemic cell death.