Two-, three-, four-, five-, and twelve-week-old gerbils were subjected
to various periods of bilateral carotid occlusion (BCO). Rectal and c
ranial temperatures were maintained at 37 degrees C during BCO, and on
ly rectal temperature was monitored for 30 min of reperfusion. Seven d
ays after ischemia, animals were perfusion-fixed and the neuronal dens
ities in the hippocampal CA1 subfields were counted. The extent of cer
ebral ischemia during BCO was evaluated with [C-14]iodoantipyrine auto
radiography. The rectal temperature spontaneously fell to 33-34 degree
s C during reperfusion in 2-week-old gerbils, although animals over 3
weeks old presented postischemic hyperthermia. Two-week-old animals th
erefore were divided into three experimental groups: In one group (2-w
eek-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, respecti
vely, during reperfusion. Five-minute BCO produced almost complete des
truction 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. [C-14]Iodoantipyrine autoradiogr
aphy revealed that BCO produced severe forebrain ischemia in 2-week-ol
d gerbils as well as in 12-week-old gerbils. These findings indicate t
hat developing gerbils have a greater tolerance to cerebral ischemia a
nd that such ischemic tolerance is not due to a collateral network bet
ween the vertebrobasilar and the carotid circulations previously repor
ted to develop more abundantly in developing gerbils.