Nuclear binding sites for triiodothyronine in the gerbil brain following ischemia and recirculation.
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.
D000818:Animals; D002545:Brain Ischemia / Q000378:metabolism*; D002467:Cell Nucleus / Q000378:metabolism*; D002540:Cerebral Cortex / Q000378:metabolism*; D002560:Cerebrovascular Circulation; D005849:Gerbillinae; D007700:Kinetics; D011956:Receptors, Cell Surface / Q000378:metabolism*; D011988:Receptors, Thyroid Hormone; D014284:Triiodothyronine / Q000378:metabolism*
D011956:Receptors, Cell Surface; D011988:Receptors, Thyroid Hormone; D014284:Triiodothyronine