Parkinson's disease (PD) is a progressive neurodegenerative disorder in which dopaminergic (DAergic) systems are destroyed (particularly in the nigrostriatal system), causing both motor and non-motor symptoms. Hippocampal neuroplasticity is altered in PD animal models, resulting in non-motor dysfunctions. However, little is known about the precise mechanism underlying the hippocampal dysfunctions in PD. Therefore, this study attempted to analyze behavioral impairments and alteration of structural plasticity in the hippocampus, as well as explain their correlations in this animal model. Striatal 6- hydroxydopamine (6-OHDA) infusions were performed unilaterally in adult SD rats. Both motor and non-motor symptoms alongside the expression of tyrosine hydroxylase (TH) in the substantia nigra and striatum were confirmed in 6-OHDA-lesioned rats. The neuronal architecture in the hippocampus was analyzed by Golgi staining. During the 7–8 weeks after infusion, the 6-OHDA-lesioned rats exhibited motor and non-motor dysfunctions (especially anxiety/depression-like behaviors). Rats with unilateral 6-OHDA infusion displayed reduced TH+ immunoreactivity in the ipsilateral nigrostriatal pathway of the brain. Golgi staining revealed that striatal 6-OHDA infusion significantly decreased the dendritic complexity (i.e., number of crossing dendrites, total dendritic length, and branch points) in the ipsilateral hippocampal CA1 apical/basal and DG subregions. Additionally, the dendritic spine density and morphology were significantly altered in the CA1 apical/basal and DG subregions following striatal 6-OHDA infusion. However, alteration of microglial and astrocytic distributions did not occur in the hippocampus following striatal 6-OHDA infusion. Furthermore, RNA-sequencing demonstrated no significant alterations in neuroinflammation-related genes in the hippocampus between sham-operated controls and 6-OHDA-lesioned rats. These findings demonstrate that in a PD animal model, inhibiting the DAergic pathway causes changes to the neuronal architecture in the hippocampus, independently of neuroinflammation. Consequently, this study provides anatomical evidence that structural plasticity in the hippocampus may play a role in the etiology of the non-motor hallmarks of PD. Key words: 6-hydroxydopamine; Dopaminergic system; Golgi staining; Non-motor symptom; Parkinson’s disease; Structural plasticity