Hypothermia reduces the propensity of cortical tissue to propagate direct current depolarizations in the rat.

Both spreading depression (SD) and spontaneous cortical ischemic depolarizations are known to be sensitive to brain temperature. What is unknown is whether this temperature effect is caused by altered sensitivity of cortical tissue to the initiating stimulus or is attributable to an altered ability of cortex to propagate the depolarization wave. To address this, halothane anesthetized rats underwent surface heating/cooling to produce pericranial temperatures of 33 degrees C, 38 degrees C, or 40 degrees C. Spreading depression was first initiated by electrocortical stimulation and then by topical application of KCl. The electrical threshold for SD and the time to direct current shift onset after KCl administration were unaffected by temperature. In contrast, the ability of cortical tissue to propagate the SD wave was temperature dependent. Decreasing temperature from 40 degrees C to 33 degrees C was associated with a slowing of the rate of propagation by 25-30% while the duration of the propagated direct current (DC) shifts was increased by 80% regardless of the initiating stimulus. After elicitation of persistent local DC shift with KCl, the interval between initial waves of SD was progressively increased as temperature was decreased. For either method of stimulation, once SD was initiated, the amplitude of the waveform was temperature independent. These results confirm the importance of temperature regulation in procedures examining SD in vivo. Further, temperature effects on SD reflect propensity of the tissue to propagate depolarization waves although ability of cortex to depolarize in direct response to the stimulus does not undergo substantive change.