Deficits in adult hippocampal neurogenesis (AHN) is a common feature in depression and Parkinson’s Disease (PD). Actually, depressive disturbances occur in 40–50% of patients with PD, influencing many clinical aspects of the disease. Indeed, PD patients and mice models exhibited fewer proliferating cells in the subventricular zone and dentate gyrus (DG). Since both regions comprise dopaminergic innervation and inputs from the nigrostriatal areas, it is plausible that dopaminergic system may exert some control over or under cytogenic brain regions.To investigate this, we used a transgenic rat (glial fibrillary acidic protein (GFAP)-thymidine kinase (TK)) model, in which the administration of an antiviral drug, Ganciclovir for 18 days resulted in abrogation of hippocampal cytogenesis. Also, apart from the reduced hippocampal newborn cells, those animals were lesioned with a unilateral intracranial injection of 6-hydroxydopamine in the striatum. Subsequently, we characterized the anxiety/depressive-like behavior, as well as their motor behavioral performance. Immature neurons and dopaminergic neurons were also quantitively assessed. Results revealed that cytogenesis abrogation may potentiate the anxiety/depressive-like phenotype of PD rats and further diminish the population of immature neurons residing in the DG, indicating that the modulation of neurogenesis may have a role in the functional performance of PD. As so, understanding the impact of the modulation of AHN and the role of non-motor symptomatology in PD may allow us to study early cellular/molecular and functional alterations promoted by age-related events. If so, novel perspectives about new potential mechanisms and therapeutic targets could be opened for PD.