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Plants with neurotoxic potential in undernourished subjects
2019, Revue NeurologiqueCitation Excerpt :Free intracellular calcium ions can activate calcium-dependent proteases that are able to destroy cellular integrity. Despite evidence that L-BOAA induces AMPA receptor-mediated motor neuronal degeneration in cell culture [48,53,54], human lathyrism primarily involves degeneration of the axonal projections of cortical motor neurons in the distal spinal cord. Betz cell loss is questionable [47], and there is no evidence of spinal anterior horn cell degeneration, either in cases of recent onset or in established cases [55].
New insights into the mechanism of neurolathyrism: L-β-ODAP triggers [Ca<sup>2+</sup>]<inf>i</inf> accumulation and cell death in primary motor neurons through transient receptor potential channels and metabotropic glutamate receptors
2014, Food and Chemical ToxicologyCitation Excerpt :The mechanism of action of L-β-ODAP has been studied from the viewpoint of excitotoxicity. The neurolathylogen L-β-ODAP is a more potent agonist of α-amino-3-hydroxy-5-methyl-4-isoxazole-4-propionic acid (AMPA)/kainate receptors than of N-methyl-D-aspartate (NMDA) receptors in vertebrate neurons (Pearson and Nunn, 1981), L-β-ODAP causes excitotoxicity in a gross manner similar to a series of natural toxins like kainate, ibotenic acid, willardiine or quisqualic acid. However, the precise receptor/channel(s) and pathways responsible for the toxicity of L-β-ODAP in motor neurons have not been fully elucidated.
Unraveling the mechanism of β-N-oxalyl-α,β-diaminopropionic acid (β-ODAP) induced excitotoxicity and oxidative stress, relevance for neurolathyrism prevention
2011, Food and Chemical ToxicologyCitation Excerpt :The first described and best documented effect is its activation of AMPA receptors as a glutamate-analogue. This effect has been reported in vitro in mouse spinal neurons (Watkins et al., 1966; Pearson and Nunn, 1981; Macdonald and Morris, 1984) and cortical neurons (Ross and Spencer, 1987; Weiss et al., 1989), cerebellar granule cells (Staton and Bristow, 1997), rodent synaptosomes (Ross and Spencer, 1987; Bridges et al., 1988; Bridges et al., 1989) and in Retzius neurons of the leech (Cemerikic et al., 2001). It was also confirmed in rat hippocampal slices (Bridges et al., 1991) and in vivo in rat and human hippocampus (Kunig et al., 1994; Kusama-Eguchi et al., 2010) and in newborn mice (Ross and Spencer, 1987; Spencer et al., 1987).
Chapter 18 Toxic disorders of the upper motor neuron system
2007, Handbook of Clinical Neurology