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  • Taking together findings from our study and

    2024-07-10

    Taking together findings from our study and that from the literature, we propose a model (to be experimentally confirmed) of possible intracellular mechanism of NA-induced regulation of Na-K ATPase subunit expression (Fig. 8). NA acting on α1-AR modulates the α1- and α3-subunit expressions of Na-K ATPase, while acting on β-AR induces the expression of β1-subunit in Neuro-2a cells. It is interesting CCT137690 that NA has opposite effect on C6-glial cells in modulating Na-K ATPase expression; NA by acting on β-AR inhibits the enzyme activity and reduces Na-K ATPase α2-subunit expression (Amar et al., 2017). This NA-induced opposite effect on neurons and glia possibly helps the CCT137690 to maintain its excitable state. We acknowledge that various post-transcriptional and post-translational modifications of tissue specific isoforms of Na-K ATPase play a crucial role in regulating Na-K ATPase subunit expression (Blanco, 2005; Therien and Blostein, 2000), which need detailed, including in vivo investigations; the findings of this study would form the basis for undertaking such studies. As physiological significance of the findings of this study, we propose the following. The Na-K ATPase regulates ionic gradient across the neuronal membrane and thus, maintains excitability status of neurons (Larsen et al., 2016). REMS loss has been reported to increase NA-level, which in turn increases Na-K ATPase activity and thus, the brain excitability and functioning are altered (Mallick and Singh, 2011). However, the molecular mechanism of how the elevated NA sustains increased Na-K ATPase activity, particularly under chronic condition, to maintain the symptoms of REMS-loss associated disorder(s) was unknown. The findings of this study are expected to help better understand REMS loss associated disorders and management of such patients.
    Conflict of interest
    Authors’ contributions
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    Acknowledgments MA received fellowship from the University Grants Commission. Research funding from Indian agencies viz. Institutional grants under Department of Biotechnology-BUILDER; Department of Science and Technology-PURSE and −FIST; University Grants Commission –Networking and –DRS, Departmental research support under UPE; and individual grant research funding to BNM from Department of Science and Technology; University Grants Commission and J C Bose Fellowship are acknowledged.