Abstract
Neurotrauma assumes an instant or delayed disconnection of axons (axotomy), which affects not only neurons, but surrounding glia as well. Not only mechanically injured glia near the site of disconnection, especially transection, is subjected to the damage, but also glia that is remote from the lesion site. Glial cells, which surround the neuronal body, in turn, support neuron survival, so there is a mutual protection between neuron and glia. Calcium signaling is a central mediator of all post-axotomy events, both in neuron and glia, playing a critical role in their survival/regeneration or death/degeneration. The involvement of calcium in post-axotomy survival of the remote, mechanically intact glia is poorly studied. The purpose of this review is to sum up the calcium-involving mechanisms in responses of neurons and glial cells to axotomy to show their importance and to give some suggestions for future research of remote glia in this context.
Highlights
Traumatic injuries to the central nervous system affect young and middle age people causing premature death and disability [1,2]
In response to peripheral nerve damage, a number of interconnected processes occurs in neuron and satellite glia. This includes the coupling of satellite glial cells, increase in ectopic spontaneous neuronal spiking and abrupt changing in electrical characteristics of neurons and glia [40], glial proliferation, and increase in glia–glial interaction via gap junctions [27,41]
In cortical neurons, when protein kinase C (PKC) is inhibited by staurosporin or PKC41, the activation of calpain leads to import of extracellular Ca2+ through the hyperpolarization-activated plasma membrane channel HNC2
Summary
Traumatic injuries to the central nervous system (brain and spinal cord) affect young and middle age people causing premature death and disability [1,2]. The injury-induced focal permeability leads to local Ca2+ influx with activation of cysteine proteases, calpain and caspases, which play an important role in resulting pathogenesis of traumatic axon injury via the proteolytic cleavage of cerebral spectrin, one of the components of subaxolemmal cytoskeleton. During this pathological process, a local calcium overload, together with calpain activation, causes mitochondrial damage, resulting in the release of cytochrome c and caspase activation. The exact role of Ca2+, including extracellular calcium, the different mechanisms of cytosolic Ca2+ regulation (Ca2+ channels and pumps), and Ca2+-activated proteins in the survival and death of RGC are still unclear
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