Two-, three-, four-, five-, and twelve-week-old gerbils were subjected to various periods of bilateral carotid occlusion (BCO). Rectal and cranial temperatures were maintained at 37 degrees C during BCO, and only rectal temperature was monitored for 30 min of reperfusion. Seven days after ischemia, animals were perfusion-fixed and the neuronal densities in the hippocampal CA1 subfields were counted. The extent of cerebral ischemia during BCO was evaluated with [14C]iodoantipyrine autoradiography. The rectal temperature spontaneously fell to 33-34 degrees C during reperfusion in 2-week-old gerbils, although animals over 3 weeks old presented postischemic hyperthermia. Two-week-old animals therefore were divided into three experimental groups: In one group (2-week-old group I) rectal temperature was not regulated during 30 min of reperfusion, while in the other two groups (2-week-old groups II and III) rectal temperature was regulated at 37 and 38 degrees C, respectively, during reperfusion. Five-minute BCO produced almost complete destruction of the CA1 neurons in 12-week-old animals. In contrast, most CA1 neurons survived 30 min of BCO in 2-week-old group I and 15 min of BCO in 2-week-old groups II and III. [14C]Iodoantipyrine autoradiography revealed that BCO produced severe forebrain ischemia in 2-week-old gerbils as well as in 12-week-old gerbils. These findings indicate that developing gerbils have a greater tolerance to cerebral ischemia and that such ischemic tolerance is not due to a collateral network between the vertebrobasilar and the carotid circulations previously reported to develop more abundantly in developing gerbils.