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Rapid action of Triiodothyronine on Mitochondrial H+, Ca2+ and Mg2+-Dependent ion Transporters in Cortex, Hippocampus and Cerebellum of Restraint Mice


Affiliations
1 Department of Zoology, School of Life Sciences, University of Kerala, Kariavattom, Thiruvananthapuram – 695 581, Kerala, India
2 Inter-University Centre for Evolutionary and Integrative Biology (iCEIB), School of Life Sciences, University of Kerala, Kariavattom, Thiruvananthapuram – 695 581, Kerala, India
     

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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 (T3) 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 (T3; 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 T3 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 T3 treatment in both non-stressed and restraint-stressed mice. The mCa2+-ATPase activity in the cortex and cerebellum decreased to significant levels after T3 treatment in both non-stressed and restraint-stressed mice. The mCa2+-ATPase activity in the hippocampus that increased to significant levels after T3 treatment, showed a reversal after restraint-stress in T3-treated mice. The mitochondrial Mg2+-ATPase activity in the cortex decreased to significant levels after T3 treatment in restraint-stressed mice. On the contrary, T3 treatment in restraint stressed mice increased to significant levels the mitochondrial Mg2+-ATPase activity in the cerebellum. The mitochondrial Mg2+-ATPase activity in the hippocampus, which increased to significant levels after T3 treatment in non-stressed mice, reversed its activity in T3-treated restraint-stressed mice. Spatial and differential action of T3 on the mitochondrial ion transporters has been found in the present study that corroborates with a rapid modulatory action of T3 on the transport of H+, Ca2+ and Mg2+ in the brain mitochondria of mice which appears to be sensitive to restraint stress.

Keywords

Brain, Mice, Mitochondrial Ca2+, H+, Mg2+ATPase, Restraint Stress, Triiodothyronine.
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  • Rapid action of Triiodothyronine on Mitochondrial H+, Ca2+ and Mg2+-Dependent ion Transporters in Cortex, Hippocampus and Cerebellum of Restraint Mice

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Authors

S. Simi
Department of Zoology, School of Life Sciences, University of Kerala, Kariavattom, Thiruvananthapuram – 695 581, Kerala, India
K. Manish
Inter-University Centre for Evolutionary and Integrative Biology (iCEIB), School of Life Sciences, University of Kerala, Kariavattom, Thiruvananthapuram – 695 581, Kerala, India
M. C. Subhash Peter
Department of Zoology, School of Life Sciences, University of Kerala, Kariavattom, Thiruvananthapuram – 695 581, Kerala, India

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 (T3) 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 (T3; 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 T3 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 T3 treatment in both non-stressed and restraint-stressed mice. The mCa2+-ATPase activity in the cortex and cerebellum decreased to significant levels after T3 treatment in both non-stressed and restraint-stressed mice. The mCa2+-ATPase activity in the hippocampus that increased to significant levels after T3 treatment, showed a reversal after restraint-stress in T3-treated mice. The mitochondrial Mg2+-ATPase activity in the cortex decreased to significant levels after T3 treatment in restraint-stressed mice. On the contrary, T3 treatment in restraint stressed mice increased to significant levels the mitochondrial Mg2+-ATPase activity in the cerebellum. The mitochondrial Mg2+-ATPase activity in the hippocampus, which increased to significant levels after T3 treatment in non-stressed mice, reversed its activity in T3-treated restraint-stressed mice. Spatial and differential action of T3 on the mitochondrial ion transporters has been found in the present study that corroborates with a rapid modulatory action of T3 on the transport of H+, Ca2+ and Mg2+ in the brain mitochondria of mice which appears to be sensitive to restraint stress.

Keywords


Brain, Mice, Mitochondrial Ca2+, H+, Mg2+ATPase, Restraint Stress, Triiodothyronine.

References





DOI: https://doi.org/10.18311/jer%2F2019%2F26221