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Evaluating the role of Adrenergic compounds on Synaptosomal Na+ -K + -ATPase and Ca2+/Mg2+ -ATPase

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ISSN 2348-313X (Print) International Journal of Life Sciences Research ISSN 2348-3148 (online) Vol. 10, Issue 2, pp: (33-40), Month: April - June 2022, Available at: www.researchpublish.com

Evaluating the role of Adrenergic compounds on Synaptosomal Na+-K+-ATPase and Ca2+/Mg2+-ATPase during Central Thyroid Hormone Homeostasis Samita Kundu1*, Sumedha Roy2, Angshuman Biswas3, Arun K. Ray4 1*

Post-Graduate Department of Zoology, Vivekananda College, Thakurpukur, Kolkata, India 2

Ex-Assistant Professor, The University of Burdwan, West Bengal, India.

3

Department of Zoology, Sreegopal Banerjee College, Hooghly, West Bengal, India. 4

Division of Molecular Medicine, Bose Institute, Kolkata, India DOI: https://doi.org/10.5281/zenodo.6598548 Published Date: 31-May-2022

Abstract: Hypothyroidism is associated with significant symptoms and an adverse effect on the quality of life. There exists a central homeostatic mechanism in the adult mammalian brain to defer these adverse neuropsychological manifestations, for some days. Thyroid hormone is known to affect the activities of some enzymes involved in neurotransmission. In this study, a reflection of the physiological consequences of ‘central thyroid hormone homeostasis’ has been addressed with the study of the activities of the synaptosomal membrane Na+-K+-ATPase and Ca2+/Mg2+-ATPase on the days of onset and termination of the homeostatic phenomenon. Moreover, certain adrenergic receptor (α2- and β-) agonists and antagonists have profound influence on synaptosomal thyroid hormone levels during the days of initiation and termination of the ‘central homeostasis’. This notion has further prompted us to investigate the effects of these compounds on Na+-K+-ATPase and Ca2+/Mg2+-ATPase during the start and end days of this central homeostatic phenomenon. The altered activities of these enzymes on these two days point towards their dependency on cerebral thyroid hormone levels and thus the hormonal involvement in neurobiochemical events. The entire phenomenon of homeostasis thus appears to be a stress-mediated event involving an array of adrenergic non-genomic effects, further indicating a nongenomic role of thyroid hormone during homeostasis. Keywords: Synaptosome, Na+-K+-ATPase, Ca2+/Mg2+-ATPase, thyroid hormone, homeostasis.

I. INTRODUCTION The adult mammalian brain can maintain a normal level of thyroid hormone (TH) up to a certain duration despite ensuing peripheral hypothyroidism. This novel homeostatic mechanism or the „central thyroid hormone (TH) homeostasis‟ has the onset between the 1st and 2nd day of anti-thyroid drug treatment, continues for 16-18 days and ends between the 18th and 20th day [1]. This „central homeostasis‟ serves to defend the adverse neuropsychological manifestations commonly associated with peripheral hypothyroidism, for a certain length of time. Chronic and acute hypothyroidism are associated with a spectrum of psychobehavioural disorders, involving derangements in neurotransmitter metabolism and function [2].

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