EN
Parkinson’s disease (PD) is a neurodegenerative disorders causing not only motor dysfunction, but also cognitive disturbance. The pattern of cognitive deficits in PD often includes: executive impairments, episodic memory deficits and visuospatial dysfunctions. It also became evident that inflammatory processes play an important role in the pathophysiology of PD. Neurodegeneration intense brain immune activation and “cytokine storm” which might induce hyper-excitability of neuronal circuits and might reduce neuronal plasticity and cause impairments in learning and memory abilities. The role of cytokines in regulation of inflammatory responses in different brain regions during PD is unclear. It still remains to be fully understood as to how cytokines participate in the molecular and cellular mechanisms of deficits in learning, memory and cognition in PD. Loss of dopaminergic neurons in acute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) models is associated with massive and prolonged glial response and increased production and release of inflammatory mediators. To assess the inflammatory response following MPTP intoxication, we measured the IL-6, IL-1β and TNFα gene expression by real-time quantitative RT-PCR following the Morris water maze behavioral test that was provided at 7 days, 3 and 6 months from the intoxication. Our results indicate that neuroinflammatory activity in MPTP model was not restricted to the nigrostriatal system but also involved hippocampal and cortical areas, regions there are essential for cognitive functions such as working and long - term memory, not only in mice. To evaluate spatial learning and memory abilities of mice the mean latency of reaching the platform, the swimming distance, the time spent in the goal quadrant and crossing parameters were estimated. We found that these parameters correlated with level of mRNA expression of cytokines in hippocampus and cortex.