Document Detail

Autophagic degeneration of motor neurons in a model of slow glutamate excitotoxicity in vitro.
MedLine Citation:
PMID:  16257859     Owner:  NLM     Status:  MEDLINE    
There is increasing evidence that so-called "autophagic cell death" participates in cell degeneration in certain pathological conditions. Autophagy might be involved in some neurodegenerative processes, including lateral amyotrophic sclerosis (SLA). The exact mechanism leading to progressive motor neuron (MN) loss remains unclear, but glutamate-mediated mechanism is thought to be responsible. Previous ultrastructural studies by the authors performed on a model of SLA in vitro, based on chronic glutamate excitotoxicity, revealed a subset of morphological features characteristic to different modes of neuronal death, including autophagic degeneration. The contribution of this pathway of MNs death is evaluated in organotypic cultures of rat lumbar spinal cord chronically exposed to specific glutamate uptake blockers: DL-threo-beta-hydroxyaspartate (THA) and L-transpyrrolidine-2,4-dicarboxylate (PDC). The study documents the various steps of authophagy in slowly evolving process of MN neurodegeneration. The cells undergoing autophagy usually exhibited sequestration of some parts of cytoplasm with normal and/or degenerated organelles, whereas other parts of cytoplasm as well as neuronal nucleus remained unchanged. The advanced autophagic changes were often associated with other modes of MN death, especially with apoptosis. Numerous MNs revealed apoptotic nuclear features with typical peripheral margination of nuclear chromatin, accompanied by severe autophagic or autophagic-necrotic degeneration of the cytoplasm. These results support the opinion of unclear distinction between different modes of cell death and indicate the involvement of autophagey in MNs neurodegeneration in vitro.
Ewa Matyja; Anna Taraszewska; Ewa Nagańska; Janina Rafałowska
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Ultrastructural pathology     Volume:  29     ISSN:  0191-3123     ISO Abbreviation:  Ultrastruct Pathol     Publication Date:    2005 Sep-Oct
Date Detail:
Created Date:  2005-10-31     Completed Date:  2005-12-13     Revised Date:  2009-06-26    
Medline Journal Info:
Nlm Unique ID:  8002867     Medline TA:  Ultrastruct Pathol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  331-9     Citation Subset:  IM    
Department of Experimental and Clinical Neuropathology, Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland.
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MeSH Terms
Amyotrophic Lateral Sclerosis / pathology
Animals, Newborn
Apoptosis / drug effects
Aspartic Acid / analogs & derivatives,  pharmacology
Autophagy / drug effects*
Dicarboxylic Acids / pharmacology
Disease Models, Animal
Excitatory Amino Acid Antagonists / pharmacology*
Glutamic Acid / metabolism
Microscopy, Electron
Motor Neurons / drug effects*,  ultrastructure
Nerve Degeneration*
Neurotransmitter Uptake Inhibitors / pharmacology*
Organ Culture Techniques
Organelles / ultrastructure
Pyrrolidines / pharmacology
Spinal Cord / drug effects*,  pathology,  ultrastructure
Reg. No./Substance:
0/Dicarboxylic Acids; 0/Excitatory Amino Acid Antagonists; 0/Neurotransmitter Uptake Inhibitors; 0/Pyrrolidines; 1860-87-3/3-hydroxyaspartic acid; 56-84-8/Aspartic Acid; 56-86-0/Glutamic Acid; 99319-03-6/pyrrolidine-2,4-dicarboxylic acid

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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