By Denson G. Fujikawa (auth.), Denson G. Fujikawa (eds.)
This publication is the results of a convergence of medical information about mechanisms that produce acute nerve cellphone loss of life within the mind. even though probably disparate, stroke, mind and spinal twine trauma, coma from a low serum glucose focus (hypoglycemia), and lengthy epileptic seizures have in universal the inciting issue of excitotoxicity, the activation of a particular subtype of glutamate receptor by way of an increased extracellular glutamate focus that leads to an over the top inflow of calcium into nerve cells. The excessive calcium focus in nerve cells prompts numerous enzymes which are accountable for degradation of cytoplasmic proteins and cleavage of nuclear DNA, leading to nerve mobilephone demise. The excessive calcium focus additionally interferes with mitochondrial respiratory, with the ensuing creation of loose radicals that harm mobile membranes and nuclear DNA. realizing the biochemical pathways that produce nerve telephone loss of life is step one towards devising a good neuroprotective method, the last word goal.
Acute Neuronal damage could be worthy to neuroscientists and common mobilephone biologists attracted to mobile demise. The e-book can be necessary to clinically orientated neuroscientists, together with neurologists, neurosurgeons and psychiatrists.
About the Editor:
Dr. Denson Fujikawa is an accessory Professor of Neurology on the David Geffen tuition of medication at UCLA, a member of the mind examine Institute at UCLA and a employees Neurologist on the division of Veterans Affairs better la Healthcare method. His curiosity in mechanisms of nerve telephone dying within the mind all started in the course of a two-year epilepsy examine fellowship with Dr. Claude Wasterlain, from 1981 to 1983. he's a Fellow of the yankee Academy of Neurology and is a member of the yank Epilepsy Society, American Neurological organization, foreign Society for Cerebral Blood circulation and Metabolism, and the Society for Neuroscience.
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Additional info for Acute Neuronal Injury: The Role of Excitotoxic Programmed Cell Death Mechanisms
Tavernarakis degradation and clumping of nuclear DNA, the formation of small, tightly wrapped membrane whorls, the rupture of the plasma membrane and the appearance of autophagosomes (Edinger and Thompson 2004). The word necrosis is derived from the Greek expression “necros,” standing for “dead” and was traditionally considered as the chaotic breakdown of the cell. In humans, necrotic cell death accompanies prolonged hypoxia, ischemia, hypoglycemia, toxin exposure, exposure to reactive oxygen metabolites, extreme changes in temperature, and nutrient deprivation (Nicotera et al.
Tavernarakis Miramar MD, Costantini P, Ravagnan L, Saraiva LM, Haouzi D, Brothers G, Penninger JM, Peleato ML, Kroemer G, Susin SA (2001) NADH oxidase activity of mitochondrial apoptosisinducing factor. J Biol Chem 276:16391–16398 Modjtahedi N, Giordanetto F, Madeo F, Kroemer G (2006) Apoptosis-inducing factor: vital and lethal. Trends Cell Biol 16:264–272 Munoz-Pinedo C, Guio-Carrion A, Goldstein JC, Fitzgerald P, Newmeyer DD, Green DR (2006) Different mitochondrial intermembrane space proteins are released during apoptosis in a manner that is coordinately initiated but can vary in duration.
It now seems clear that the above-described apoptosis versus necrosis dichotomy is an artificial division, and that “programmed” cell death is a more complex physiological process than initially thought. The cell can use different mechanisms/ pathways with underlying apoptotic or necrotic features to accomplish its proper S. A. G. 1007/978-0-387-73226-8_3, © Springer Science+Business Media, LLC 2010 35 36 S. A. Susin demise in a controlled manner (Jaattela 2002; Broker et al. 2005; Jaattela and Tschopp 2003; Okada and Mak 2004; Golstein and Kroemer 2007; Golstein et al.
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