Parkinson's disease (PD) is neurodegenerative disorder characterized by progressive loss of dopamine(DA)rgic neurons in the substantia nigra pars compacta (SNpc). The most obvious symptoms are movement-related behavioral deficits. In advanced stages of the disease, thinking and retrieval deficits often arise from cognitive impairments. However, the mechanism of cognitive disorder in PD remains largely unknown. In the present study, we investigated the mechanism of cognitive deficits resulting from loss of the nigrostriatal DArgic neurons. PD model mouse (PD mouse) was produced by intraperitoneal administration of 1-methyl-4-phenyl-1, 2, 3, 6, tetrahydropyridine (four injections at a single dose of 20 mg/kg every 2 h), which destroys specifically the DArgic neurons in the SNpc, and the number of tyrosine hydroxylase positive cells in the SNpc was significantly decreased in PD mice. We evaluated the cognitive function of PD mice by the contextual fear conditioning test (CFCT). In CFCT, mice were trained with the footshock as unconditioned stimulus (US) in a training box (context) as conditioned stimulus (CS) and, 24 h latar, reexposed to CS for 3 min (for reconsolidation) or 30 min (for extinction) without US. Memory (freezing) was assessed by placing mice once again in CS 24 h after reexposure. In extinction memory test under weak US (1 mA/2 s, single), there was no significant difference in freezing rate between control and PD mice. In reconsolidation memory test, however, PD mice showed significant reduction of freezing rate compared to the control. Next we carried out the experiment under more intense US (2 mA/2 s, twice). In this test, reconsolidation of PD mice normally occurred. However, the memory of PD mice was attenuated earlier than control by brief exposure to CS (3 min) every day. These results suggest that PD mice show not only impairment of reconsolidation but also enhancement of extinction.