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(Stroke. 2001;32:788.)
© 2001 American Heart Association, Inc.

Original Contributions

Electrophysiological Properties of CA1 Neurons Protected by Postischemic Hypothermia in Gerbils

H. Dong, PhD; F. Moody-Corbett, PhD; F. Colbourne, PhD; Q. Pittman, PhD D. Corbett, PhD

From the Neuroscience Research Group and Department of Physiology and Biophysics, University of Calgary, Calgary, Alberta (H.D., Q.P.); Basic Medical Sciences, Faculty of Medicine, Memorial University, St John’s, Newfoundland (F.M-C., D.C.); and Department of Psychology, University of Alberta, Edmonton, Alberta (F.C.), Canada.

Correspondence to Dr Dale Corbett, Basic Medical Sciences, Faculty of Medicine, Memorial University, St John’s, Newfoundland, Canada A1B 3V6. E-mail corbett{at}mun.ca

Background and Purpose—Recent studies show that prolonged (eg, 24-hour) postischemic hypothermia confers lasting histological and behavioral protection against severe global cerebral ischemia. However, functional abnormalities may be compensated for by undamaged brain regions and thus not detected by behavioral tests. To determine whether hypothermia preserves CA1 functional integrity, we measured synaptic and membrane properties of CA1 neurons in ischemic gerbils treated with postischemic hypothermia.

Methods—Gerbils were subjected to 5 minutes of forebrain ischemia and were either left untreated or exposed to 2 days of hypothermia (32°C for 24 hours and then 34°C for 24 hours). Sham animals were operated on but not made ischemic, then either allowed to recover at room temperature or subjected to hypothermia for 2 days. Approximately 5 weeks after ischemia or sham surgery, patch-clamp recordings were obtained from the CA1 region of hippocampal slices.

Results—There was approximately 95% CA1 cell loss in untreated ischemic animals, whereas ischemic gerbils treated with hypothermia had cell counts similar to sham animals. Resting membrane potential, action potential amplitude and duration, input resistance, and synaptic currents evoked by Schaffer collateral stimulation were similar between pyramidal cells obtained from ischemic 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 support for the use of hypothermia as a treatment for cerebral ischemia.

Key Words: cerebral ischemia, global • hippocampus • hypothermia • neuroprotection • gerbils

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