Study on the distribution of FOSB and nNOs proteins after metoclopramide-induced oromandibular dyskinesia in C57Bl/6 mice
The study of the nitrergic system in the side effects caused by the blockade of the dopamine D2 receptor, such as catalepsy and tardive dyskinesia, has been explored by our group in Swiss mice. Understanding a little better the interaction of the nitrergic system with the dopaminergic system leads us to think that there must be a target molecule, such as the DARPP-32 protein in medium-sized spinous neurons in the striatum, which regulates the information sent by the striatum-nigral and striatum-pallidal efferences, involved in hyperkinetic/dyskinetic or akinetic effects, respectively. In the present study we intend to study the immunoreactivity of FosB, nNOS, GFAP proteins in the cingular cortex, striatum and substantia nigra, after induction of tardive dyskinesia with metoclopramide (Plasil®) in C57Bl/6 mice. We also intend to describe and correlate with the behavior the astrocytic activation that occurs through its participation in the synapses of this region. In the first phase, with behavior, it was demonstrated that Metoclopramide caused motor disorders of hypokinesia, such as catalepsy, and hyperkinesia, such as Vacuous Chewing Movement (VCM), at both doses 5-> 25 and 8mg/kg when compared to the group control. For the continuation of the study, it is necessary to complete the immunoreactivity evaluations of the proposed markers.