We investigated the role of GABAergic parvalbumin-expressing (PV) interneurons in the hippocampus in spatial and hippocampus-dependent memory abilities in rat models of Parkinson's disease (PD). Experiments were performed in adult male Wistar rats, including physiological controls(n=14) and toxin lesion-induced PD models: PD cholinopathy(n=10), hemiparkinsonism(n=7), and hemiparkinsonism with PD cholinopathy(n=6). Behavioral assessments and PV immunohistochemistry were performed 14 and 42 days after the lesions. Spatial and hippocampus-dependent short- and long-term memory were assessed with the spatial habituation test and the novel object recognition test. All experimental groups had no motor impairments during the follow-up period (X2≥2.01,p≥0.07). Although PV expression in the hippocampus remained unchanged over time in PD cholinopathy (z≥-1.91,p≥0.06), we detected impairments in spatial, short- and long-term recognition memory, but only at day 42 (X2≥0.38,p=0.83;t=0.13,p=0.91). In the hemiparkinsonian rats, unchanged hippocampal PV expression (z≥-1.52,p≥0.14) was followed by impaired spatial memory (X2≥2.87,p≥0.22), but both recognition memories were intact over time (t≥3.16,p≤0.03). In the hemiparkinsonian rats with PD cholinopathy, long-lasting impairment of spatial memory (X2≥0.72,p≥0.22) was followed by delayed short- and long-term impairment of recognition memory (t=-0,24,p=0.82) along with hippocampal PV suppression (z=-3.17,p=10-3), which was functionally coupled with recognition memory impairment (r=0.52,p=0.04). Our results suggest that dopaminergic denervation plays an important role in the impairment of spatial memory in the prodromal stage of PD, while cholinergic denervation and hippocampal PV suppression impair short-term and long-term memory in PD with cholinopathy and hemiparkinsonism with PD cholinopathy in a delayed manner.