The effect of cerebral ischemia and subsequent recirculation on the nuclear 
thyroid hormone receptors was investigated. Ischemia was produced by occlusion 
of the right common carotid artery in the Mongolian gerbil. The thyroid hormone 
receptors were measured in vitro by a [125I]triiodothyrorine (T3) binding assay 
with isolated nuclei and Scatchard analysis. A rapid increase of the total 
number of binding sites for T3 appeared within 30 min of ischemia and reached 
over 40% by 3 h. During the same 3-h period, the relative binding affinity was 
reduced by 25%. Upon recirculation after 30 min or 3 h of ischemia, a rapid 
reversal of measured T3 binding sites occurred, which progressed to 20-30% below 
the control value by the recirculation period of 3 h. If the ischemic period was 
only 30 min, the nuclear T3 binding capacity recovered toward the control level 
and the affinity constant returned normal after recirculation for 24 h. When the 
ischemic period was extended to 3 h, there was progressive loss of receptor 
sites, and no tendency for recovery of the affinity constant was observed. These 
results demonstrated a prompt alteration of a specific nuclear regulatory 
component in cerebral ischemia, which may indicate the importance of such 
changes within the nuclear regulatory mechanism for reversibility of cerebral 
function following ischemic insult.