Rapid action of Triiodothyronine on Mitochondrial H + , Ca 2+ and Mg 2+ -Dependent ion Transporters in Cortex, Hippocampus and Cerebellum of Restraint Mice

Abstract

Thyroid hormones (TH) have a multitude of actions, mainly on development and differentiation during early life and play many vital roles in almost all tissues including neuronal tissues. TH rapidly alters the mitochondrial functions both by its genomic and direct actions on mitochondrial binding sites. The functional relationship between TH and mitochondrial ion transport during stress response has not yet been elucidated in mammals so far. Here, we report a rapid in vivo action of triiodothyronine (T 3 ) on mitochondrial ion transporter functions in the neuronal clusters of cortex, hippocampus and cerebellum of Swiss Albino mouse ( Mus musculus ) treated short-term with triiodothyronine (T 3 ; 200ng g-1) for 30 min either in non-stressed or in restraint-stressed (30 min each day for 7 days). The mH + -ATPase activity in the cortex decreased to significant levels after T 3 treatment in both non-stressed and restraint-stressed mice. On the contrary, the mH + -ATPase activity in the hippocampus and cerebellum increased to significant levels after T 3 treatment in both non-stressed and restraint-stressed mice. The mCa 2+ -ATPase activity in the cortex and cerebellum decreased to significant levels after T 3 treatment in both non-stressed and restraint-stressed mice. The mCa 2+ -ATPase activity in the hippocampus that increased to significant levels after T 3 treatment, showed a reversal after restraint-stress in T 3 -treated mice. The mitochondrial Mg 2+ -ATPase activity in the cortex decreased to significant levels after T 3 treatment in restraint-stressed mice. On the contrary, T 3 treatment in restraint stressed mice increased to significant levels the mitochondrial Mg 2+ -ATPase activity in the cerebellum. The mitochondrial Mg 2+ -ATPase activity in the hippocampus, which increased to significant levels after T 3 treatment in non-stressed mice, reversed its activity in T 3 -treated restraint-stressed mice. Spatial and differential action of T 3 on the mitochondrial ion transporters has been found in the present study that corroborates with a rapid modulatory action of T 3 on the transport of H + , Ca 2+ and Mg 2+ in the brain mitochondria of mice which appears to be sensitive to restraint stress.