V-006 | Behavioral effects of yerba mate on L-DOPA induced dyskinesia in a mouse model of Parkinson’s disease

Cellular and Molecular Neurobiology
Author: Andrea Cecilia Cura | Email: cecilia.cura@uner.edu.ar

Andrea Cecilia Cura^1°, Liliana Teresita Tribbia^1°,Florencia Echeverria^1°, Lorena Rela^2°3°, Irene Rita Eloísa Taravini^1°

^1° Laboratorio de Neurobiología Experimental. LNE-ICTAER-UNER-CONICET, Gualeguaychú, Entre Ríos, Argentina.
^2° Universidad de Buenos Aires, Facultad de Medicina, Departamento de Ciencias Fisiológicas, Grupo de Neurociencia de Sistemas, Ciudad de Buenos Aires, Argentina.
^3° CONICET, Universidad de Buenos Aires, Instituto de Fisiología y Biofísica Bernardo Houssay (IFIBIO Houssay), Buenos Aires, Argentina

Current pharmacological therapy for Parkinson’s disease (PD) focuses on the administration of L-DOPA, but after several years it promotes the emergence of L-DOPA-induced dyskinesia (LID). LID is very difficult to reverse, can be more disabling than the underlying disease, and correlates with inflammation and oxidative stress. Yerba mate (YM) consumption is inversely related to PD and has anti-inflammatory and anti-oxidant effects.
Our aim is to investigate whether YM consumption has a preventive effect attenuating LID development in a mouse model of PD. We performed two experiments using mice with severe lesions to the nigrostriatal system by administration of 6-OHDA in the medial forebrain bundle: (1) Chronic YM treatment: mice received an infusion of YM per oral for 2 months, then were lesioned and continued with the treatment along with the administration of L-DOPA, for 15 days; (2) Co-administration of YM with L-DOPA: mice were first lesioned and then received YM via gastric gavage, 1 hour prior to the injection of L-DOPA, for 15 days. In both experiments control groups (sham and water) received vehicle. Our preliminary results suggest that YM administration to severely denervated animals, in both experiments, could reduce the severity of LID compared to control animals. It remains to be evaluated whether this behavioral benefit correlates with a reversal of the maladaptive striatal synaptic plasticity and changes in microglial and astrocytic reactivity observed in LID.