Paper Report for: Rodriguez-Ithurralde_1995_J.Neurol.Sci_129_104
Reference
Title: Glutamate-receptor elicited acetylcholinesterase release in mouse spinal cord slice: a model of early excitotoxic injury Rodriguez-Ithurralde D, Olivera S, Migues V, Vincent O, Salazar R Ref: Journal of the Neurological Sciences, 129:104, 1995 : PubMed
To investigate the mechanisms by which glutamate-induced acetylcholinesterase (AChE) release might play a part in the pathogenesis of excitotoxically triggered motor neurone disease, we measured AChE molecular forms released after glutamate-receptor agonist stimulation of superfused and incubated slices of mouse spinal cord. Kainate and GLU caused a dose-related, calcium-dependent, magnesium-blocked liberation of AChE soluble forms (mainly G4) from both the ventral and dorsal horns, without membrane damage. In the immature slice, glycine potentiated GLU elicited AChE release in the presence of strychnine, suggesting N-methyl-D-aspartate (NMDA) receptor involvement. After the 30th postnatal day, nearly all the release was caused by non-NMDA receptor stimulation. The response might interfere with the negative feedback loop which modulates the overactivation of motor neurones, and might render them more vulnerable to excitotoxic stress.
        
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Rodriguez-Ithurralde D, Olivera S, Migues V, Vincent O, Salazar R (1995) Glutamate-receptor elicited acetylcholinesterase release in mouse spinal cord slice: a model of early excitotoxic injury Journal of the Neurological Sciences129: 104-6
Rodriguez-Ithurralde D, Olivera S, Migues V, Vincent O, Salazar R (1995) Journal of the Neurological Sciences129: 104-6