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Journal of Thyroid Research
Volume 2013 (2013), Article ID 457953, 9 pages
Research Article

Mechanisms of L-Triiodothyronine-Induced Inhibition of Synaptosomal Na+-K+-ATPase Activity in Young Adult Rat Brain Cerebral Cortex

1Department of Basic Sciences, Parker University, 2500 Walnut Hill Lane, Dallas, TX 75229, USA
2Center for Computational & Integrative Biology, Rutgers University, 315 Penn Street, Camden, NJ 08102, USA
3Department of Molecular Medicine, Bose Institute, P-1/12, CIT, Scheme VII-M, Calcutta 700054, India

Received 29 June 2013; Revised 19 September 2013; Accepted 24 September 2013

Academic Editor: Noriyuki Koibuchi

Copyright © 2013 Pradip K. Sarkar et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The role of thyroid hormones (TH) in the normal functioning of adult mammalian brain is unclear. Our studies have identified synaptosomal Na+-K+-ATPase as a TH-responsive physiological parameter in adult rat cerebral cortex. L-triiodothyronine (T3) and L-thyroxine (T4) both inhibited Na+-K+-ATPase activity (but not Mg2+-ATPase activity) in similar dose-dependent fashions, while other metabolites of TH were less effective. Although both T3 and the β-adrenergic agonist isoproterenol inhibited Na+-K+-ATPase activity in cerebrocortical synaptosomes in similar ways, the β-adrenergic receptor blocker propranolol did not counteract the effect of T3. Instead, propranolol further inhibited Na+-K+-ATPase activity in a dose-dependent manner, suggesting that the effect of T3 on synaptosomal Na+-K+-ATPase activity was independent of β-adrenergic receptor activation. The effect of T3 on synaptosomal Na+-K+-ATPase activity was inhibited by the -adrenergic agonist clonidine and by glutamate. Notably, both clonidine and glutamate activate -proteins of the membrane second messenger system, suggesting a potential mechanism for the inhibition of the effects of TH. In this paper, we provide support for a nongenomic mechanism of action of TH in a neuronal membrane-related energy-linked process for signal transduction in the adult condition.