Maintenance of homeostasis for thyroid hormone in the adult rat brain: possible involvement of a nuclear-mediated phenomenon.
During adult-onset peripheral hypothyroidism, the brain maintains normal levels of thyroid hormone for some time through a mechanism of 'central homeostasis'. Although onset, duration, and termination of such a homeostatic phenomenon have been recently evaluated in rat models, the mechanism behind remains unknown. During our investigation to understand the mechanism further, we injected the protein synthesis blockers actinomycin D and cycloheximide along with propylthiouracil to adult male rats during the days of onset (day 2) and termination (day 20) of the homeostatic mechanism. We evaluated synaptosomal T(3) level and neuronal Na(+)-K(+)-ATPase and acetylcholinesterase activities along with deiodinase II activity and cyclic adenosine monophosphate level in the cerebral cortex. The results indicated prevalence of unchanged or lower levels of synaptosomal T(3) on the 2nd and on the 20th day, respectively. Such a condition has been parallely supported by reflections in cerebrocortical deiodinase II activity and cyclic adenosine monophosphate levels. The activities of cerebrocortical synaptosomal Na(+)-K(+)-ATPase and acetylcholinesterase, which are the two important physiological parameters for neuronal function, have been found to be supportive of the involvement of a neuronal protein-mediated factor in the 'on' and 'off' reactions in central homeostasis during peripheral hypothyroidism. The results of our study indicate that the expression of 'central thyroid hormone homeostasis' is a genomic nuclear-mediated mechanism.
Kundu
Samita
S
Department of Animal Physiology, Bose Institute, Calcutta, India.
Roy
Sumedha
S
De
Jhuma
J
Biswas
Angshuman
A
Pramanik
Mitali
M
Ray
Arun K
AK
D000110:Acetylcholinesterase / Q000378:metabolism; D000367:Age Factors; D000818:Animals; D013956:Antithyroid Agents / Q000494:pharmacology; D002467:Cell Nucleus / Q000502:physiology; D002540:Cerebral Cortex / Q000378:metabolism*; D000242:Cyclic AMP / Q000378:metabolism; D003513:Cycloheximide / Q000494:pharmacology; D003609:Dactinomycin / Q000494:pharmacology; D006706:Homeostasis / Q000502:physiology*; D007037:Hypothyroidism / Q000139:chemically induced / Q000378:metabolism*; D007453:Iodide Peroxidase / Q000378:metabolism; D008297:Male; D011441:Propylthiouracil / Q000494:pharmacology; D011500:Protein Synthesis Inhibitors / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D013574:Synaptosomes / Q000201:enzymology; D013974:Thyroxine / Q000096:biosynthesis / Q000097:blood / Q000378:metabolism*; D014284:Triiodothyronine / Q000096:biosynthesis / Q000097:blood / Q000378:metabolism*; D000097564:Iodothyronine Deiodinase Type II
D000110:Acetylcholinesterase; D013956:Antithyroid Agents; D000242:Cyclic AMP; D003513:Cycloheximide; D003609:Dactinomycin; D007453:Iodide Peroxidase; D011441:Propylthiouracil; D011500:Protein Synthesis Inhibitors; D000254:Sodium-Potassium-Exchanging ATPase; D013974:Thyroxine; D014284:Triiodothyronine; D000097564:Iodothyronine Deiodinase Type II