This dissertation investigates compensatory mechanisms at the pre and post synaptic level in an animal model of Parkinson's disease (PD). The maintenance of dopamine (DA) tone despite neurodegeneration of the nigrostriatal pathway seen in PD has been the main explanation for the absence of Parkinsonian symptoms. In Chapter 1 an appropriate literature review on the topic of PD in the context of compensatory mechanisms is presented. In Chapter 2 we have demonstrated further evidence in support of the compensatory model of 'passive stabilization' in an animal model of preclinical PD. Moreover, evidence of a new neurochemical deficit associated with phasic signaling, thought to result in transient DA release (known as DA transients) at the terminal level, is presented. In Chapter 3 in vivo voltammetry and extracellular single unit electrophysiology is "time shared" for elucidation of a functional concentration of DA. Electrophysiological effect of electrically evoked DA mimicking DA transients presumably associated with phasic signaling on striatal units is quantified in a concentration-effect plot, from which a functional concentration of DA is obtained. The functional concentration was found to be in close proximity to known concentrations of behaviorally evoked DA transients. Based on our results from Chapter 2 and 3, where a deficit in phasic signaling and functional concentration of DA is presented, Chapter 4 focuses on the investigation of a compensatory mechanism downstream to the neurochemical deficit in phasic signaling at the striatal target cells. Changes in functional concentration were used as a measure of compensation and were found to decrease in moderate (preclinical PD) and severe (clinical PD) lesion groups. These results indicate that compensation may exist in the preclinical phase of PD, thus explaining the absence of symptoms despite neurochemical deficit. Chapter 5 is dedicated to establishing a new model for studying established models (long term depression (LTD) or potentiation) of memory formation in the striatum. We have preliminary data indicating that the new model of LTD formation is DA dependent and that it is partially mediated via D₂-receptors.