这本书是关于大脑中产生急性神经细胞死亡的机制的科学信息汇集的结果。虽然看似不同，但中风、脑和脊髓损伤、低血糖浓度（低血糖）引起的昏迷和长时间的癫痫发作都是兴奋毒性的共同诱因，即细胞外谷氨酸浓度升高激活特定的谷氨酸受体亚型，导致钙过多流入神经细胞。
神经细胞中的高钙浓度激活了几种酶，这些酶负责细胞质蛋白质的降解和核DNA的切割，导致神经细胞死亡。高钙浓度还会干扰线粒体呼吸，从而产生自由基，破坏细胞膜和核DNA。了解导致神经细胞死亡的生化途径是设计有效的神经保护策略的第一步，也是最终目标。
急性神经元损伤将有助于神经科学家和对细胞死亡感兴趣的普通细胞生物学家。这本书也将有助于面向临床的神经学家，包括神经学家、神经外科医生和精神病医生。
关于编辑
藤川丹森博士是加州大学洛杉矶分校大卫·格芬医学院的神经学兼职教授，加州大学洛杉矶分校大脑研究所成员，也是一名Sta
退伍军人事务部大洛杉矶医疗系统神经科医师。他对大脑神经细胞死亡机制的兴趣始于1981年至1983年与克劳德·瓦斯特兰博士进行的为期两年的癫痫研究。他是美国神经科学院院士，也是美国癫痫学会、美国神经学会、国际脑血流与代谢学会和神经科学学会的成员。
Acute Neuronal Injury: The Role of Excitotoxic Programmed Cell Death Mechanisms by Denson G. Fujikawa
This book is the result of a convergence of scientific information regarding mechanisms that produce acute nerve cell death in the brain. Although seemingly disparate, stroke, brain and spinal cord trauma, coma from a low serum glucose concentration (hypoglycemia), and prolonged epileptic seizures have in common the inciting factor of excitotoxicity, the activation of a specific subtype of glutamate receptor by an elevated extracellular glutamate concentration that results in an excessive influx of calcium into nerve cells.
The high calcium concentration in nerve cells activates several enzymes that are responsible for degradation of cytoplasmic proteins and cleavage of nuclear DNA, resulting in nerve cell death. The high calcium concentration also interferes with mitochondrial respiration, with the resultant production of free radicals that damage cellular membranes and nuclear DNA. Understanding the biochemical pathways that produce nerve cell death is the first step toward devising an effective neuroprotective strategy, the ultimate goal.
Acute Neuronal Injury will be useful to neuroscientists and general cell biologists interested in cell death. The book will also be helpful to clinically oriented neuroscientists, including neurologists, neurosurgeons and psychiatrists.
About the Editor
Dr. Denson Fujikawa is an Adjunct Professor of Neurology at the David Geffen School of Medicine at UCLA, a member of the Brain Research Institute at UCLA and a Sta
ff Neurologist at the Department of Veterans Affairs Greater Los Angeles Healthcare System. His interest in mechanisms of nerve cell death in the brain began during a two-year epilepsy research fellowship with Dr. Claude Wasterlain, from 1981 to 1983. He is a Fellow of the American Academy of Neurology and is a member of the American Epilepsy Society, American Neurological Association, International Society for Cerebral Blood Flow and Metabolism, and the Society for Neuroscience.
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