Evidence for Synaptic Apoptosis
Increasing evidence indicates that neurons die by apoptosis, an active form of cell death involving a relatively stereotyped series of biochemical changes that culminate in nuclear fragmentation, in many different developmental and pathophysiological settings. In contrast to most other cell types, n...
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Published in | Experimental neurology Vol. 153; no. 1; pp. 35 - 48 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
Amsterdam
Elsevier Inc
01.09.1998
Elsevier |
Subjects | |
Online Access | Get full text |
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Abstract | Increasing evidence indicates that neurons die by apoptosis, an active form of cell death involving a relatively stereotyped series of biochemical changes that culminate in nuclear fragmentation, in many different developmental and pathophysiological settings. In contrast to most other cell types, neurons have elaborate morphologies with complex neuritic arbors that often extend great distances from the cell body. Neuronal death signals are likely to be activated at remote synaptic sites and, indeed, overactivation of glutamate receptors and underactivation of trophic factor receptors are implicated in neurodegenerative disorders. We now report that biochemical changes consistent with apoptosis are engaged locally in synapses. Exposure of cortical synaptosomes to staurosporine and Fe2+resulted in loss of membrane phospholipid assymetry, caspase activation, and mitochondrial alterations (membrane depolarization, calcium overload, and oxyradical accumulation) characteristic of apoptosis. The caspase inhibitor zVAD-fmk prevented mitochondrial membrane depolarization in synaptosomes. Studies of the effects of cytosolic extracts from synaptosomes exposed to apoptotic insults, on isolated nuclei, showed that signals capable of inducing nuclear apoptosis are generated locally in synapses. Exposure of cultured hippocampal neurons to staurosporine and glutamate resulted in caspase activation and mitochondrial membrane depolarization in dendrites, and zVAD-fmk prevented the membrane depolarization. Glutamate-induced increases in caspase activity were first observed in dendrites and later in the cell body, and focal application of glutamate to individual dendrites resulted in local activation of caspases. Collectively, the data demonstrate that apoptotic biochemical cascades can be activated locally in synapses and dendrites and suggest a role for such local apoptotic signals in synapse loss and neuronal death in neurodegenerative disorders that involve excessive activation of glutamate receptors. |
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AbstractList | Increasing evidence indicates that neurons die by apoptosis, an active form of cell death involving a relatively stereotyped series of biochemical changes that culminate in nuclear fragmentation, in many different developmental and pathophysiological settings. In contrast to most other cell types, neurons have elaborate morphologies with complex neuritic arbors that often extend great distances from the cell body. Neuronal death signals are likely to be activated at remote synaptic sites and, indeed, overactivation of glutamate receptors and underactivation of trophic factor receptors are implicated in neurodegenerative disorders. We now report that biochemical changes consistent with apoptosis are engaged locally in synapses. Exposure of cortical synaptosomes to staurosporine and Fe2+resulted in loss of membrane phospholipid assymetry, caspase activation, and mitochondrial alterations (membrane depolarization, calcium overload, and oxyradical accumulation) characteristic of apoptosis. The caspase inhibitor zVAD-fmk prevented mitochondrial membrane depolarization in synaptosomes. Studies of the effects of cytosolic extracts from synaptosomes exposed to apoptotic insults, on isolated nuclei, showed that signals capable of inducing nuclear apoptosis are generated locally in synapses. Exposure of cultured hippocampal neurons to staurosporine and glutamate resulted in caspase activation and mitochondrial membrane depolarization in dendrites, and zVAD-fmk prevented the membrane depolarization. Glutamate-induced increases in caspase activity were first observed in dendrites and later in the cell body, and focal application of glutamate to individual dendrites resulted in local activation of caspases. Collectively, the data demonstrate that apoptotic biochemical cascades can be activated locally in synapses and dendrites and suggest a role for such local apoptotic signals in synapse loss and neuronal death in neurodegenerative disorders that involve excessive activation of glutamate receptors. Increasing evidence indicates that neurons die by apoptosis, an active form of cell death involving a relatively stereotyped series of biochemical changes that culminate in nuclear fragmentation, in many different developmental and pathophysiological settings. In contrast to most other cell types, neurons have elaborate morphologies with complex neuritic arbors that often extend great distances from the cell body. Neuronal death signals are likely to be activated at remote synaptic sites and, indeed, overactivation of glutamate receptors and underactivation of trophic factor receptors are implicated in neurodegenerative disorders. We now report that biochemical changes consistent with apoptosis are engaged locally in synapses. Exposure of cortical synaptosomes to staurosporine and Fe2+ resulted in loss of membrane phospholipid asymmetry, caspase activation, and mitochondrial alterations (membrane depolarization, calcium overload, and oxyradical accumulation) characteristic of apoptosis. The caspase inhibitor zVAD-fmk prevented mitochondrial membrane depolarization in synaptosomes. Studies of the effects of cytosolic extracts from synaptosomes exposed to apoptotic insults, on isolated nuclei, showed that signals capable of inducing nuclear apoptosis are generated locally in synapses. Exposure of cultured hippocampal neurons to staurosporine and glutamate resulted in caspase activation and mitochondrial membrane depolarization in dendrites, and zVAD-fmk prevented the membrane depolarization. Glutamate-induced increases in caspase activity were first observed in dendrites and later in the cell body, and focal application of glutamate to individual dendrites resulted in local activation of caspases. Collectively, the data demonstrate that apoptotic biochemical cascades can be activated locally in synapses and dendrites and suggest a role for such local apoptotic signals in synapse loss and neuronal death in neurodegenerative disorders that involve excessive activation of glutamate receptors. |
Author | Keller, Jeffrey N. Begley, James G. Mattson, Mark P. |
Author_xml | – sequence: 1 givenname: Mark P. surname: Mattson fullname: Mattson, Mark P. – sequence: 2 givenname: Jeffrey N. surname: Keller fullname: Keller, Jeffrey N. – sequence: 3 givenname: James G. surname: Begley fullname: Begley, James G. |
BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1581220$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/9743565$$D View this record in MEDLINE/PubMed |
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ISSN | 0014-4886 |
IngestDate | Fri Aug 16 07:18:59 EDT 2024 Thu Sep 12 19:55:36 EDT 2024 Thu May 23 23:01:26 EDT 2024 Sun Oct 29 17:08:29 EDT 2023 Fri Feb 23 02:34:39 EST 2024 |
IsPeerReviewed | true |
IsScholarly | true |
Issue | 1 |
Keywords | staurosporine synaptosomes mitochondrial transmembrane potential Alzheimer's disease dendritic spines glutamate oxidative stress caspase Oxidative stress Rat Rodentia Nervous system Glutamate Mechanism Vertebrata Synapse Synaptosome Mammalia Neuron Cell death Animal Apoptosis |
Language | English |
License | CC BY 4.0 Copyright 1998 Academic Press. |
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PublicationDate | 1998-09-01 |
PublicationDateYYYYMMDD | 1998-09-01 |
PublicationDate_xml | – month: 09 year: 1998 text: 1998-09-01 day: 01 |
PublicationDecade | 1990 |
PublicationPlace | Amsterdam |
PublicationPlace_xml | – name: Amsterdam – name: United States |
PublicationTitle | Experimental neurology |
PublicationTitleAlternate | Exp Neurol |
PublicationYear | 1998 |
Publisher | Elsevier Inc Elsevier |
Publisher_xml | – name: Elsevier Inc – name: Elsevier |
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SubjectTerms | Alzheimer's disease Animals Annexin A5 - metabolism Apoptosis - physiology Biological and medical sciences Biomarkers Blotting, Western Calcium - metabolism caspase Caspase 3 Caspases Cell Nucleus - drug effects Cell Nucleus - ultrastructure Cell-Free System Cells, Cultured Cysteine Endopeptidases - metabolism Cysteine Proteinase Inhibitors - pharmacology dendritic spines Development. Senescence. Regeneration. Transplantation Female Fundamental and applied biological sciences. Psychology glutamate Glutamic Acid - pharmacology Hippocampus - cytology Hippocampus - physiology Hippocampus - ultrastructure Membrane Potentials - physiology mitochondrial transmembrane potential Neurons - physiology Neurons - ultrastructure oxidative stress Rats Rats, Sprague-Dawley Reactive Oxygen Species - metabolism staurosporine Synapses - physiology Synapses - ultrastructure synaptosomes Synaptosomes - physiology Synaptosomes - ultrastructure Vertebrates: nervous system and sense organs |
Title | Evidence for Synaptic Apoptosis |
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