Calcium Mobilization within Hypothyroid Adult Rat Brain Synaptosomes

Introduction

Thyroid hormones (TH) influence the growth and development of the maturing mammalian brain via specific nuclear receptors, while their role in normal functioning of the adult mammalian brain is unclear. However, adult-onset of dysthyroidism develops a number of functional and neuropsychological disorders in adult humans [1]. In contrast to the developing brain, most of the changes developed in adults are reversible with the proper adjustment of circulatory TH.

Recently, the idea of direct non-genomic actions of TH in adult neurons  is interesting. These include distribution, concentration, metabolism and binding of L-triiodothyronine (L-T₃) [1] [2] in the synaptosomes of adult rat cerebral cortex and indicate crucial role of TH in neuronal functions in adult mammals. Although TH-mediated calcium entry in adult rat brain synaptosomes [3] [4], and in hypothyroid mouse cerebral cortex [5] have been reported, its synaptic functions in adult neurons in dysthyroidism are unclear. Calcium-influx is an important physiological function in brain, following which cascades of membrane events occur that ultimately lead to neurotransmitter release and follow up neural functions. Disruption in this crucial membrane event may lead to various neuropsychological disorders that depend on calcium. Present study demonstrates a regulation and homeostatic mechanism of calcium accumulation within cerebrocortical synaptosomes of hypothyroid adult rat.

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