Electrophysiological properties of CA1 neurons protected by postischemic hypothermia in gerbils

Background and Purpose-Recent studies show that prolonged leg. 24-hour) pos tischemic hypothermia confers lasting histological and behavioral protectio n against severe global cerebral ischemia. However, functional abnormalitie s may be compensated for by undamaged brain regions and thus not detected b y behavioral tests. To determine whether hypothermia preserves CA1 function al integrity, we measured synaptic and membrane properties of CA1 neurons i n ischemic gerbils treated with postischemic hypothermia. Methods-Gerbils were subjected to 5 minutes of forebrain ischemia and were either left untreated or exposed to 3 days of hypothermia (32 degreesC for 24 hours and then 34 degreesC for 24 hours). Sham animals were operated on but not made ischemic, then either allowed to recover at room temperature o r subjected to hypothermia for 2 days. Approximately 5 weeks after ischemia or sham surgery, patch-clamp recordings were obtained from the CAI legion of hippocampal slices. Results-There was approximately 95% CA1 cell loss in untreated ischemic ani mals, whereas ischemic gerbils treated with hypothermia had cell counts sim ilar to sham animals. Resting membrane potential, action potential amplitud e and duration, input resistance, and synaptic currents evoked by Schaffer collateral stimulation were similar between pyramidal cells obtained from i schemic gerbils treated with hypothermia and sham-operated animals (P>0.05) . Conclusions-These data demonstrate that postischemic hypothermia preserves the measured electrophysiological properties of CA1 neurons in the absence of any apparent functional abnormalities. This study provides further suppo rt for the use of hypothermia as a treatment for cerebral ischemia.