Spontaneous postischemic hyperthermia is not required for severe CA1 ischemic damage in gerbils.

We have recently shown that brain temperature can drop even though rectal and skull readings are maintained near 37 degrees C during global forebrain ischemia in the gerbil. In this study gerbils were subjected to 5 min of ischemia followed by 85 min of extended halothane anesthesia, while rectal and skull temperatures were kept at normal values. This extended anesthesia procedure prevented the development of spontaneous postischemic hyperthermia. However, it occasionally produced mild brain hypothermia both during ischemia and throughout anesthesia. In addition, the degree of brain hypothermia positively correlated with CA1 preservation; with some gerbils showing complete protection. In contrast, animals with normal brain temperature displayed extensive CA1 cell loss. These data suggest that postischemic hyperthermia is not a prerequisite for extensive CA1 loss in gerbils exposed to 5 min of ischemia. Second, rectal and skull recordings are not always reliable indicators of brain temperature, especially during anesthesia.

Temperature changes associated with forebrain ischemia in the gerbil.

Changes in brain temperature during and following ischemia have not been systematically examined in the gerbil. In this study, gerbils were subjected to a 5-min bilateral carotid artery occlusion. During surgery, skull and body temperatures were maintained with a heated water blanket and a homeothermic blanket unit, respectively. Rectal, skull and brain temperatures were monitored throughout ischemia and for up to 3 h in the post-ischemic period. Intra-ischemic brain temperature fell by approximately 1.5 degrees C even though skull and rectal temperatures remained at normal values. Since brain temperature modulates the extent of ischemic injury it may not be sufficient to rely on skull and/or rectal temperature readings, especially during periods of anesthesia.

Impaired acquisition of the Morris water maze following global ischemic damage in the gerbil.

Five minutes of global ischemia in the Mongolian gerbil impaired acquisition of a Morris water maze task when testing began 72 h after surgery. In spite of extensive damage to CA1 pyramidal cells, ischemic animals eventually learned to locate a submerged platform and performed normally on a subsequent retention test. Animals that were allowed a more protracted recovery period (21 days) acquired the task as readily as control gerbils. These results suggest that undamaged structures within and external to the hippocampal formation allow spatial learning to proceed at a somewhat reduced rate.