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Calcium and Neuronal Death in Spinal Neurons

  • Chapter
Neurobiology of Spinal Cord Injury

Part of the book series: Contemporary Neuroscience ((CNEURO))

Abstract

Spinal cord trauma can result in the death of neurons both immediately after injury and several hours afterwards. The cause of immediate neuronal death is thought to be mechanical impact, but delayed neuronal damage is believed to be caused by ischemia secondary to decreased spinal cord blood flow, hemorrhage, and edema (198). The resultant neuronal death is thought to involve calcium entry similar to focal ischemic brain injuries. The predominant hypotheses on the mechanisms by which Ca2+-dependent neurodegeneration is triggered are discussed in the context of current understanding of physiologic and pathologic Ca2+ signaling. Specifically, we address whether measurable relationships exist between Ca2+ influx and neurotoxicity, whether Ca2+ excess is a sufficient trigger for neurotoxicity, and whether Ca2+ neurotoxicity is a function of Ca2+ ion concentration, spatial distribution, and influx pathway. We focus primarily on the factors that relate cellular Ca2+ ions to the requirements for triggering neurotoxicity.

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Chu, G.K.T., Tator, C.H., Tymianski, M. (2000). Calcium and Neuronal Death in Spinal Neurons. In: Kalb, R.G., Strittmatter, S.M. (eds) Neurobiology of Spinal Cord Injury. Contemporary Neuroscience. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-200-5_2

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