Excitotoxicity and cholinergic chemical markers during programmed motor neurone death.
We measured cholinergic markers and acetylcholinesterase (AChE) molecular forms after glutamate receptor stimulation of superfused slices of mouse spinal cord at different developmental ages. AChE globular forms were secreted in a dose-dependent fashion. A period of selective sensitivity to excitotoxic agents was detected by increased acetylcholine (ACh) release and AChE secretion (sAChE) at postnatal day 14. Strychnine-resistant glycine stimulation potentiated glutamate-induced AChE release, suggesting N-methyl-D-aspartate (NMDA) receptor involvement.
Rodríguez-Ithurralde
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Division of Neuromyology, Instituto de Investigaciones Biológicas Clemente Estable (IIBCE), Montevideo, Uruguay.
Vincent
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D000109:Acetylcholine / Q000378:metabolism; D000110:Acetylcholinesterase / Q000378:metabolism; D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D015415:Biomarkers; D018846:Excitatory Amino Acids / Q000633:toxicity*; D018698:Glutamic Acid / Q000378:metabolism; D051379:Mice; D009046:Motor Neurons / Q000201:enzymology / Q000378:metabolism* / Q000502:physiology; D010275:Parasympathetic Nervous System / Q000201:enzymology / Q000378:metabolism*; D017470:Receptors, Glutamate / Q000187:drug effects / Q000378:metabolism / Q000502:physiology; D013116:Spinal Cord / Q000166:cytology / Q000201:enzymology / Q000378:metabolism
D015415:Biomarkers; D018846:Excitatory Amino Acids; D017470:Receptors, Glutamate; D018698:Glutamic Acid; D000110:Acetylcholinesterase; D000109:Acetylcholine