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 mobilephone dying within the mind. even though likely disparate, stroke, mind and spinal wire 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 selected 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 a number of enzymes which are answerable for degradation of cytoplasmic proteins and cleavage of nuclear DNA, leading to nerve cellphone dying. The excessive calcium focus additionally interferes with mitochondrial breathing, with the consequent creation of unfastened radicals that harm mobile membranes and nuclear DNA. knowing the biochemical pathways that produce nerve phone demise is step one towards devising a good neuroprotective method, the last word goal.
Acute Neuronal harm can be important to neuroscientists and normal cellphone biologists drawn to mobilephone dying. The publication may 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 tuition of drugs at UCLA, a member of the mind examine Institute at UCLA and a employees Neurologist on the division of Veterans Affairs higher l. a. Healthcare method. His curiosity in mechanisms of nerve telephone loss of life within the mind started in the course of a two-year epilepsy learn 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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Extra info for Acute Neuronal Injury: The Role of Excitotoxic Programmed Cell Death Mechanisms
In an unc-51 deficient background, necrotic cell death, triggered either by deg-3(d) or mec-4(d) or hypoxia (see the following section on necrosis for details) is significantly suppressed. This effect is also observed after downregulation of other autophagy-related genes such as bec-1, lgg-1 and atgr-18 by RNAi. In addition, increase of autophagosomes formation is observed under conditions of neurodegeneration. Calpain proteases and autophagy appear to act in the same pathway (Samara et al. 2008).
The second classification is based on the type of chromatin condensation and comprises classical apoptosis, apoptosis-like PCD, and necrosislike PCD (Jaattela and Tschopp 2003). According to this classification, apoptosis is characterized by compact (stage 2) chromatin condensation, whereas apoptosislike PCD displays partial/peripheral (stage 1) chromatin condensation. In necrosislike PCD chromatin is either noncondensed at all, or only slightly granulated (Jaattela and Tschopp 2003; Leist and Jaattela 2001).
However, several recent studies in C. elegans indicate that specific molecular mechanisms are involved in the necrotic destruction of the cell. Because necrosis is implicated in many devastating human disorders, such as neurodegenerative diseases and stroke, elucidation of the biochemical events that transpire during necrosis has the potential to provide targets for effective pharmacological interventions. In addition to the three major categories of caspase-independent cell death, novel cell death paradigms that do not involve caspase function are emerging.
Acute Neuronal Injury: The Role of Excitotoxic Programmed Cell Death Mechanisms by Denson G. Fujikawa (auth.), Denson G. Fujikawa (eds.)