Abstract
Calcium-binding proteins (CBPs) can influence and react to Ca2+ transients and modulate the activity of proteins involved in both maintaining homeostatic conditions and protecting cells in harsh environmental conditions. Hibernation is a strategy that evolved in vertebrate and invertebrate species to survive in cold environments; it relies on molecular, cellular, and behavioral adaptations guided by the neuroendocrine system that together ensure unmatched tolerance to hypothermia, hypometabolism, and hypoxia. Therefore, hibernation is a useful model to study molecular neuroprotective adaptations to extreme conditions, and can reveal useful applications to human pathological conditions. In this review, we describe the known changes in Ca2+-signaling and the detection and activity of CBPs in the nervous system of vertebrate and invertebrate models during hibernation, focusing on cytosolic Ca2+ buffers and calmodulin. Then, we discuss these findings in the context of the neuroprotective and neural plasticity mechanisms in the central nervous system: in particular, those associated with cytoskeletal proteins. Finally, we compare the expression of CBPs in the hibernating nervous system with two different conditions of neurodegeneration, i.e., platinum-induced neurotoxicity and Alzheimer’s disease, to highlight the similarities and differences and demonstrate the potential of hibernation to shed light into part of the molecular mechanisms behind neurodegenerative diseases.
Highlights
The individual cells of an organism are not isolated in a stable medium, but are immersed in an ever-changing environment influenced by both the activity of surrounding cells and the external conditions in which the organism is living
We provide an overview of the known changes in the detection and activity of calcium-binding proteins (CBPs) that have been studied and reported in the nervous system during hibernation, which is a strategy used by several invertebrate and vertebrate animals to survive in cold conditions. (i)
Given the widespread role of calcium signaling, it is not surprising that several pathologies have been correlated to alterations of normal calcium homeostasis [13,14,15,16]; since neuroprotective mechanisms have been demonstrated during hibernation, we show that studying calcium regulation in this model could reveal interesting applications to tackle human pathological conditions such as neurodegenerative diseases. (iii)
Summary
The individual cells of an organism are not isolated in a stable medium, but are immersed in an ever-changing environment influenced by both the activity of surrounding cells and the external conditions in which the organism is living. A highly conserved signaling toolkit controls the level of intracellular Ca2+: Ca2+ ions enter the cytoplasm through channels on the plasma membrane, or can be released from intracellular stores in the endoplasmic reticulum, Golgi apparatus, and mitochondria; through the activity of pumps and ion exchangers, the Ca2+ concentration can return to lower steady-state levels [8,9,10] These mechanisms allow the formation of Ca2+ transients during which Ca2+ can act directly or indirectly on several pathways by binding to calcium-binding proteins (CBPs), which interpret and respond to the transients [10,11]. Based on our expertise on the effects of cytotoxic drugs on nervous tissues [17,18,19], we try to clarify the alterations in CBPs in the case of the cytological and histological damage of the nervous system, and compare these models of neurodegeneration to the unmatched tolerance observed in the natural condition of hibernation, taking into consideration the relationship between the components of CBPs and the cytoskeleton
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