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Loss of midbrain dopaminergic neurons in Parkinson's disease not only induces motor impairments but also leads to the development of non-motor symptoms such as memory impairment, anxiety and depression. Dopaminergic axons directly innervate hippocampus and release dopamine in the local environment of hippocampus, and hence are directly involved in the modulation of hippocampal-dependent functions. Studies have explored the potential effect of dopamine on adult hippocampal neurogenesis. However, it is not well defined whether oxidative damage and inflammation could be associated with alteration in adult hippocampal neurogenesis. In the present study, we analyzed the effect of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine on adult hippocampal neurogenesis and how it is associated with inflammatory conditions in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced mouse model of Parkinson's disease-like phenotypes. 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-treated mice exhibited significantly reduced dopaminergic neurons and dopamine content that resulted in impairment of motor functions. Interestingly, the formation of endogenous neuronal precursor cells and the number of neuroblasts in the hippocampus were significantly increased following 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine treatment. Net hippocampal neurogenesis was also reduced in the hippocampus after 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine treatment. These effects in the hippocampus were associated with increased oxidative stress markers and a massive reactive gliosis. Taken together, our results suggest that degeneration of midbrain dopaminergic neurons directly affects the local hippocampal microenvironment by enhancing inflammatory influences. The 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced inflammatory reaction in the hippocampus may alter the endogenous regenerative capacity of the brain. Therefore, anti-inflammatory agents could be a potential therapy for the improvement of the endogenous regenerative capacity of the aging or neurodegenerative brain.
This article was published in the following journal.
Name: Behavioural pharmacology
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The appearance of carbonyl groups (such as aldehyde or ketone groups) in PROTEINS as the result of several oxidative modification reactions. It is a standard marker for OXIDATIVE STRESS. Carbonylated proteins tend to be more hydrophobic and resistant to proteolysis.
A protein deglycase that repairs methylglyoxal- and glyoxal-glycated amino acids and proteins, releasing repaired proteins and lactate or glycolate. It deglycates CYSTEINE, ARGININE and LYSINE residues to reactivate proteins by reversing glycation and prevent the formation of ADVANCED GLYCATION END PRODUCTS. It protects cells against OXIDATIVE STRESS and CELL DEATH by functioning as an oxidative stress sensor and redox-sensitive MOLECULAR CHAPERONE and PROTEASE. Mutations in the PARK7 gene are associated with autosomal-recessive, early-onset PARKINSON DISEASE.
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