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Ultrastructural pattern of motor‐neurone degeneration in model of slow neurotoxicity in vitro
Author(s) -
Matyja E.,
Taraszewska A.,
Nagańska E.,
Rafałowska J.
Publication year - 2003
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.85.s2.15_8.x
Subject(s) - neurotoxicity , glutamate receptor , astrocyte , amyotrophic lateral sclerosis , neurodegeneration , ultrastructure , biology , spinal cord , neuroscience , in vitro , toxicity , chemistry , microbiology and biotechnology , central nervous system , anatomy , pathology , biochemistry , medicine , receptor , disease , organic chemistry
The chronic glutamate neurotoxicity is suggested to be involved in selective loss of motor neurones (MN) in amyotrophic lateral sclerosis (ALS). Evidence indicates that the loss of MN might be in part due to defective glutamate (GLU) transport resulting in elevation of synaptic glutamate. The in vitro model of slow neurodegeneration based on inhibition of GLU transport was used to evaluate the ultrastructural characteristics of neuronal and glial toxicity. The organotypic cultures of rat lumbar spinal cord maintaining the neurone–astrocyte metabolic interactions were subjected to GLU uptake blockers: threohydroxyaspartate (THA) and l ‐transpyrrolidine‐2,4‐dicarboxylate (PDC). The MN exhibited vacuolar degeneration accompanied by presence of apoptotic profiles. The astroglial cells revealed some morphological abnormalities indicating their damage. The results suggest the involvement of both neuronal and glial components in the process of GLU‐mediated toxicity.