New PDF release: Acute Neuronal Injury: The Role of Excitotoxic Programmed

By Denson G. Fujikawa (auth.), Denson G. Fujikawa (eds.)

ISBN-10: 038773225X

ISBN-13: 9780387732251

This e-book is the results of a convergence of medical information about mechanisms that produce acute nerve telephone demise 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 means 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 liable for degradation of cytoplasmic proteins and cleavage of nuclear DNA, leading to nerve phone loss of life. The excessive calcium focus additionally interferes with mitochondrial respiratory, with the ensuing creation of loose radicals that harm mobile membranes and nuclear DNA. knowing the biochemical pathways that produce nerve mobile loss of life is step one towards devising a good neuroprotective process, the last word goal.

Acute Neuronal harm might be beneficial to neuroscientists and common mobilephone biologists attracted to phone demise. The publication can also be worthwhile 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 institution of medication at UCLA, a member of the mind learn Institute at UCLA and a employees Neurologist on the division of Veterans Affairs higher l. a. Healthcare process. His curiosity in mechanisms of nerve mobilephone demise within the mind begun in the course of a two-year epilepsy examine fellowship with Dr. Claude Wasterlain, from 1981 to 1983. he's a Fellow of the yank Academy of Neurology and is a member of the yank Epilepsy Society, American Neurological organization, foreign Society for Cerebral Blood movement 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

Sample text

Degenerins are similar in sequence to the subunits of the amiloride-sensitive epithelial Na+ channel (ENaC) in mammals (Tavernarakis and Driscoll 2001). Large side chain substitutions of amino acids close to the pore forming region of degenerins enhance sodium and calcium conductivity leading to necrotic cell death (Syntichaki and Tavernarakis 2004). Ultimately, extensive ion influx disrupts cellular Ca2+ homeostasis (Syntichaki and Tavernarakis 2003). Calcium imbalance caused by mutated ion channels triggers further release of Ca2+ from the endoplasmic reticulum (ER)via the ryanodine (RyR) and inositol-1,4,5triphosphate receptors (Ins(1,4,5)P3PR).

2002), the DNA-degrading capacity of AIF relies on the recruitment of downstream nucleases, such as cyclophilin A (cyp A) (Cande et al. 2004) or endonuclease G (EndoG) (Wang et al. 2002; Bajt et al. 2006; Whiteman et al. 2007). Necrosis-like PCD occurs by yet poorly understood molecular mechanisms, but it is usually independent of caspase activation, with some exceptions [see Edinger and Thompson (2004), Sperandio et al. (2000), Boise and Collins (2001), Meurette et al. (2007), and Zong and Thompson (2006)].

Cytoplasmic degeneration”) (Clarke 1990). Sub-type 3A is characterized by nuclear disintegration whereas sub-type 3B displays karyolysis (Clarke 1990; Beaulaton and Lockshin 1982). Above-described types 2 and 3 PCD occur without pronounced nuclear chromatin condensation. This nuclear feature is used as the main criterion to classify a given type of cell death as necrosis-like PCD (Jaattela and Tschopp 2003; Leist and Jaattela 2001). Apoptosis-like PCD can be considered as an intermediate morphological phenotype.

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Acute Neuronal Injury: The Role of Excitotoxic Programmed Cell Death Mechanisms by Denson G. Fujikawa (auth.), Denson G. Fujikawa (eds.)


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