Abstract
The term necrosis is a Greek word meaning “deadness.” A contemporary definition of necrosis is the sum of morphological changes indicative of cell death (Majno and Joris 1995). Necrosis usually applies to cell death that occurs to a group of cells or part of an organ in vivo, but the term has more recently been applied to cells in culture. Necrosis is the form of cell death which usually occurs when cells were injured by extreme physical stress or chemical challenges to the point that is beyond repair. As a result of the presence of massive ion influx (e.g., Na+, Ca2+), early and marked mitochondria swelling and cell swelling (oncosis) characterize necrosis (Majno and Joris 1995; Trump et al. 1997) (Fig. 1). Nonspecific DNA breakage results in the formation of chromatin fragments (in a punctuate fashion) all over the nuclei. Eventually, the nuclei become leaky and ultimately the plasma membrane ruptures. At least under in vitro conditions, necrosis is rapid and the time course of cell death is usually within 1–5-h death (Majno and Joris 1995).
Keywords
- Neuronal Apoptosis
- Spinal Muscular Atrophy
- Cereb Blood Flow
- Cerebellar Granule Neuron
- Experimental Traumatic Brain Injury
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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Wang, K.K.W. (2002). Limiting Apoptosis as a Strategy for CNS Neuroprotection. In: Marcoux, F.W., Choi, D.W. (eds) CNS Neuroprotection. Handbook of Experimental Pharmacology, vol 155. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-06274-6_2
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