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Nishimura, K., Kitamura, Y., Inoue, T., Umesono, Y., Sano, S., Yoshimoto, K., Inden, M., Takata, K., Taniguchi, T., Shimohama, S. and Agata, K. (2007) Reconstruction of dopaminergic neural network and locomotion function in planarian regenerates. Developmental Neurobiology, 67, 1059-1078. doi:10.1002/dneu.20377

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• TITLE: Potential of a planarian model to study certain aspects of anti-Parkinsonism drugs

  AUTHORS: Robert B. Raffa, Jeff Danah, Christopher S. Tallarida, Carrie Zimmerman, Grace Gill, Steven J. Baron, Scott M. Rawls

  KEYWORDS: L-DOPA; Benserazide; Planarians

  JOURNAL NAME: Advances in Parkinson's Disease, Vol.2 No.3, July 19, 2013

  ABSTRACT: We previously created and investigated a planarian model for the study of drug action, abuse, physical dependence, receptor affinity, the toxicity of heavy metals in wastewater, and seizures. For the present pilot study, we investigated the possibility that this model might be useful for studying certain aspects of drugs used in treatment of Parkinson disease. For the first step, we were interested in finding an in vivo metric for the inhibition of L-DOPA by an inhibitor of DOPA decarboxylase. The direct clinical relevance of the endpoint was of secondary concern during this preliminary phase of model development. Two metrics were explored: L-DOPA-induced inhibition of motility (locomotor velocity) and dopamine-mediated toxicity, which was quantified using a Kaplan-Meier survival curve. L-DOPA produced both dose- and time-related toxicity. The water-soluble DOPA decarboxylase inhibitor benserazide dose-dependently inhibited the effect of L-DOPA, as manifested by a leftward shift in the Kaplan-Meier curve. Additional work was initiated using the more sensitive and a graded metric of spontaneous locomotor velocity. The encouraging results of this pilot study suggest that: 1) planarians contain DOPA decarboxylase or an equivalent enzyme, and 2) the planarian model might be useful for the study of certain aspects of anti-Parkinsonism pharmacotherapy.