Abstract
Recent literature demonstrated that exposure to excitatory amino acid in specific experimental conditions might produce a defect in the autophagy pathway. Such an effect was observed in motor neurons exposed chronically to glutamate agonists. On the other hand, it is well known that glutamate induces motor neuron death and this is supposed to play a key role in the physiopathology of motor neuron loss in amyotrophic lateral sclerosis (ALS). Similarly, a defective recruitment of autophagy was recently documented in ALS. In the present study we found that exposure of motor neurons to kainic acid produces intracellular changes associated with defective autophagy. In this experimental conditions, pharmacological activation of autophagy rescues the loss of motor neurons.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adjuvants, Immunologic / pharmacology
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Analysis of Variance
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Animals
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Apoptosis Regulatory Proteins / metabolism
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Autophagy / drug effects*
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Beclin-1
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Cell Count / methods
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Cells, Cultured
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Dizocilpine Maleate / pharmacology
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Drug Interactions
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Embryo, Mammalian
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Excitatory Amino Acid Agonists / pharmacology
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Female
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Glutamic Acid / pharmacology*
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Kainic Acid / pharmacology
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Lithium Chloride / pharmacology
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Mice
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Microscopy, Electron, Transmission / methods
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Motor Neurons / drug effects*
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Motor Neurons / ultrastructure
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Neurofilament Proteins / metabolism
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Neuroprotective Agents / pharmacology
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Pregnancy
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Spinal Cord / cytology
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Time Factors
Substances
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Adjuvants, Immunologic
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Apoptosis Regulatory Proteins
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Beclin-1
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Becn1 protein, mouse
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Excitatory Amino Acid Agonists
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Neurofilament Proteins
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Neuroprotective Agents
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neurofilament protein H
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Glutamic Acid
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Dizocilpine Maleate
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Lithium Chloride
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Kainic Acid