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Author(s): Martin LJ; Al-Abdulla NA; Brambrink AM; Kirsch JR; Sieber FE; Portera-Cailliau C
Title: Nueurodegeneration in excitotoxicity, global cerebral ischemia, and target deprivation: A perspective on the contributions of apoptosis and necrosis
Source: BRAIN RESEARCH BULLETIN 46 (4): 281-309
Date: 1998 JUL 1
Document Type: Journal : Review
DOI:
Language: English
Comment:
Address: Johns Hopkins Univ, Sch Med, Div Neuropathol, Dept Pathol, Baltimore, MD 21205 USA.
Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Anesthesiol Crit Care Med, Baltimore, MD 21205 USA. Univ Mainz, Dept Anesthesiol, D-6500 Mainz, Germany. Reprint: Martin, LJ, Johns Hopkins Univ, Sch Med, Div Neuropathol, Dept Pathol,
558 Ross Bldg, Baltimore, MD 21205 USA. E-mail: lmartin@welchlink.welch.jhu.edu
Author Keywords: axotomy; glutamate receptor; mitochondria; oxidative injury; programmed
cell death
KeyWords Plus: DELAYED NEURONAL DEATH; PROGRAMMED CELL-DEATH; INTERNUCLEOSOMAL DNA
CLEAVAGE; TRANSIENT FOREBRAIN ISCHEMIA; AMYOTROPHIC-LATERAL-SCLEROSIS;
ELECTRON-MICROSCOPIC ANALYSIS; GLUTAMATE RECEPTOR SUBUNITS; EARLY
POSTNATAL-DEVELOPMENT; HIPPOCAMPAL CA1 NEURONS; SPINAL MUSCULAR-ATROPHY
Abstract: In the human brain and spinal cord, neurons degenerate after acute insults (e.g., stroke, cardiac arrest, trauma) and during progressive, adult-onset diseases [e.g., amyotrophic lateral sclerosis, Alzheimer's disease]. Glutamate receptor-mediated excitotoxicity has been implicated in all of these neurological conditions. Nevertheless, effective approaches to prevent or limit neuronal damage in these disorders remain elusive, primarily because of an incomplete understanding of the mechanisms of neuronal death in in vivo settings. Therefore, animal models of neurodegeneration are crucial for improving our understanding of the mechanisms of neuronal death. In this review, we evaluate experimental data on the general characteristics of cell death and, in particular, neuronal death in the central nervous system (CNS) following injury. We focus on the ongoing controversy of the contributions of apoptosis and necrosis in neurodegeneration and summarize new data from this laboratory on the classification of neuronal death using a variety of animal models of neurodegeneration in the immature or adult brain following excitotoxic injury, global cerebral ischemia, and axotomy/target deprivation. In these different models of brain injury, we determined whether the process of neuronal death has uniformly similar morphological characteristics or whether the features of neurodegeneration induced by different insults are distinct. We classified neurodegeneration in each of these models with respect to whether it resembles apoptosis, necrosis, or an intermediate form of cell death falling along an apoptosis-necrosis continuum. We found that N-methyl-D-aspartate (NMDA) receptor-and non-NMDA receptor-mediated excitotoxic injury results in neurodegeneration along an apoptosis-necrosis continuum, in which neuronal death (appearing as apoptotic, necrotic, or intermediate between the two extremes) is influenced by the degree of brain maturity and the subtype of glutamate receptor that is stimulated. Global cerebral ischemia produces neuronal death that has commonalities with excitotoxicity and target deprivation. Degeneration of selectively vulnerable populations of neurons after ischemia is morphologically nonapoptotic and is indistinguishable from NMDA receptor-mediated excitotoxic death of mature neurons. However, prominent apoptotic cell death occurs following global ischemia in neuronal groups that are interconnected with selectively vulnerable populations of neurons and also in nonneuronal cells. This apoptotic neuronal death is similar to some forms of retrograde neuronal apoptosis that occur following target deprivation. We conclude that cell death in the CNS following injury can coexist as apoptosis, necrosis, and hybrid forms along an apoptosis-necrosis continuum. These different forms of cell death have varying contributions to the neuropathology resulting from excitotoxicity, cerebral ischemia, and target deprivation/axotomy, Degeneration of different populations of cells (neurons and nonneuronal cells) may be mediated by distinct or common causal mechanisms that can temporally overlap and perhaps differ mechanistically in the rate of progression of cell death. (C) 1998 Elsevier Science Inc.
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