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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

Topiramate-antagonism of L-glutamate-induced paroxysms in planarians.

We recently reported that NMDA (N-methyl-D-aspartate) and AMPA (α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid) induce concentration-dependent paroxysms in planarians (Dugesia dorotocephala). Since the postulated mechanisms of action of the sulfamate-substituted monosaccharide antiepileptic drug topiramate include inhibition of glutamate-activated ion channels, we tested the hypothesis that topiramate would inhibit glutamate-induced paroxysms in our model. We demonstrate that: (1) L-glutamate (1-10 mM), but not D-glutamate, induced dose-related paroxysms, and that (2) topiramate dose-relatedly (0.3-3 mM) inhibited L-glutamate-induced paroxysms. These results provide further evidence of a topiramate-sensitive glutamate receptor-mediated activity in this model.[1]

References

  1. Topiramate-antagonism of L-glutamate-induced paroxysms in planarians. Raffa, R.B., Finno, K.E., Tallarida, C.S., Rawls, S.M. Eur. J. Pharmacol. (2010) [Pubmed]
 
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