Effects of right-unilateral 6-hydroxydopamine infusion-induced memory impairment and oxidative stress: relevance for Parkinson’s disease

2008 ◽  
Vol 3 (3) ◽  
pp. 250-257 ◽  
Author(s):  
Lucian Hritcu ◽  
Alin Ciobica ◽  
Vlad Artenie
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Memory Impairment ◽  
Short Term Memory ◽  
Term Memory ◽  
Shuttle Box ◽  
Y Maze ◽  
6 Hydroxydopamine ◽  
And Oxidative Stress

AbstractMale Wistar rats were subjected to right-unilateral 6-hydroxydopamine (6-OHDA) (2 μg/μl) lesions of the ventral tegmental area (VTA) or the substantia nigra (SN), or were sham-operated, and their ability to acquire the operant task was studied by means of Y-maze and shuttle-box tasks. Lesions of both the VTA and the SN resulted in an impairment of conditioned avoidance response and increase of crossing latency tested by means of shuttle-box task, suggesting significant effects of long-term memory. 6-OHDA significantly decreased spontaneous alternation in Y-maze task, suggesting effects on spatial memory, especially on short-term memory. In addition, 6-OHDA lesions of the VTA and the SN induced reductions in superoxide dismutase (SOD), glutathione peroxidase (GPX) activities and malondialdehyde (MDA) levels in the temporal lobe rather than in the frontal lobe homogenates. Our results provide further support for the toxic effects of 6-OHDA-induced memory impairment and oxidative stress with relevance for Parkinson’s disease.

scholarly journals Ketamine reversed short-term memory impairment and depressive-like behavior in animal model of Parkinson's disease

2021 ◽  
Vol 168 ◽  
pp. 63-73
Author(s):  
Débora Dalla Vecchia ◽  
Luiz Kae Sales Kanazawa ◽  
Etiéli Wendler ◽  
Palloma de Almeida Soares Hocayen ◽  
Maria Aparecida Barbato Frazão Vital ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Animal Model ◽  
Memory Impairment ◽  
Short Term Memory ◽  
Short Term ◽  
Term Memory

scholarly journals Are Proteinopathy and Oxidative Stress Two Sides of the Same Coin?

Cells ◽  
2019 ◽  
Vol 8 (1) ◽  
pp. 59 ◽  
Author(s):  
Nihar Mehta ◽  
Praneet Marwah ◽  
David Njus
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Protein Aggregation ◽  
Great Majority ◽  
Protein Aggregates ◽  
Oxidation Products ◽  
Full Picture ◽  
6 Hydroxydopamine ◽  
And Oxidative Stress

Parkinson’s disease, like other neurodegenerative diseases, exhibits two common features: Proteinopathy and oxidative stress, leading to protein aggregation and mitochondrial damage respectively. Because both protein aggregates and dysfunctional mitochondria are eliminated by autophagy, we suggest that inadequate clearance may couple the two phenomena. If a neuron’s autophagy machinery is overwhelmed, whether by excessive oxidative stress or by excessive protein aggregation, protein aggregates and dysfunctional mitochondria will both accumulate. Parkinson’s disease may provide a unique window into this because there is evidence that both sides contribute. Mutations amplifying the aggregation of α-synuclein are associated with Parkinson’s disease. Likewise, mutations in Parkin and PINK1, proteins involved in mitophagy, suggest that impaired mitochondrial clearance is also a contributing factor. Many have suggested that dopamine oxidation products lead to oxidative stress accounting for the dopaminergic selectivity of the disease. We have presented evidence for the specific involvement of hypochlorite-oxidized cysteinyl-dopamine (HOCD), a redox-cycling benzothiazine derivative. While toxins like 6-hydroxydopamine and 1-methyl-4-phenyl pyridinium (MPP+) have been used to study mitochondrial involvement in Parkinson’s disease, HOCD may provide a more physiologically relevant approach. Understanding the role of mitochondrial dysfunction and oxidative stress in Parkinson’s disease and their relation to α-synuclein proteinopathy is important to gain a full picture of the cause, especially for the great majority of cases which are idiopathic.

Nicotine-induced memory impairment by increasing brain oxidative stress

2009 ◽  
Vol 4 (3) ◽  
pp. 335-342 ◽  
Author(s):  
Lucian Hritcu ◽  
Alin Ciobica ◽  
Lucian Gorgan
Keyword(s):  
Oxidative Stress ◽  
Passive Avoidance ◽  
Memory Impairment ◽  
Short Term Memory ◽  
Memory Performance ◽  
Long Term Memory ◽  
Avoidance Task ◽  
Term Memory ◽  
Y Maze ◽  
Brain Oxidative Stress

AbstractMale Wistar rats were subjected to chronic nicotine treatment (0.3 mg/kg; 7 continuous days) and their memory performance was studied by means of Y-maze and multi-trial passive avoidance tasks. Nicotine significantly decreased spontaneous alternation in Y-maze task and step-through-latency in the multi-trial passive avoidance task, suggesting effects on both short-term memory and long-term memory, respectively. In addition, nicotine induced neuronal apoptosis, DNA fragmentation, reduced antioxidant enzymes activity, and increased production of lipid peroxidation and reactive oxygen species, suggesting pro-oxidant activity. Our results provide further support that nicotine-induced memory impairment is due to an increase in brain oxidative stress in rats.

scholarly journals Astragaloside IV Protects 6-Hydroxydopamine-Induced SH-SY5Y Cell Model of Parkinson’s Disease via Activating the JAK2/STAT3 Pathway

2021 ◽  
Vol 15 ◽  
Author(s):  
ZhengHu Xu ◽  
Dongfeng Yang ◽  
Xiaojing Huang ◽  
Huai Huang
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cell Viability ◽  
Cell Model ◽  
Astragaloside Iv ◽  
Stat3 Pathway ◽  
Apoptosis Rate ◽  
6 Hydroxydopamine ◽  
And Oxidative Stress

ObjectivesAstragaloside IV (AS-IV), the main active component of Astragalus membranaceus, bears anti-inflammatory, antioxidant, and neuroprotective activity. Parkinson’s disease (PD) is a common neurodegenerative disease. This study explored the protective effect of AS-IV on the cell model of PD.Materials and MethodsSH-SY5Y cells were incubated with different concentrations (10, 50, 100, 150, and 200 μM) of 6-hydroxydopamine (6-OHDA) for 0, 3, 6, 12, 24, and 48 h to establish the PD cell model. Different concentrations (0, 25, 50, 100, 150, and 200 μM) of AS-IV or 15 mM JAK2/STAT3 pathway inhibitor SC99 was added for intervention 2 h before 6-OHDA treatment. The viability and morphological damage of 6-OHDA-treated SH-SY5Y cells were measured using MTT assay and Hoechst 33258 staining. The expression of microtubule associated protein 2 (MAP2) was detected by immunofluorescence staining. The levels of inflammation and oxidative stress were measured using ELISA. Apoptosis of 6-OHDA-treated SH-SY5Y cells was detected using flow cytometry, and phosphorylation level of JAK2 and STAT3 were detected using Western blot analysis.ResultsThe survival rate of SH-SY5Y cells treated with 100 μM 6-OHDA for 24 h was about 50%. AS-IV (25–100 μM) significantly improved the viability (all p < 0.01), increased MAP2 expression, and repaired the morphological damage induced by 6-OHDA. AS-IV inhibited IL-1β, IL-6, and TNF-α level (all p < 0.05), reduced MDA and ROS content and increased SOD concentration, thereby reducing inflammation and oxidative stress (all p < 0.01) in 6-OHDA-treated SH-SY5Y cells. Moreover, AS-IV decreased apoptosis rate and Bax/Bcl-2 ratio induced by 6-OHDA (all p < 0.05). Mechanically, AS-IV significantly increased the phosphorylation of JAK2 and STAT3 (p < 0.01); the addition of SC99 decreased the cell viability, increased the apoptosis rate, enhanced the levels of inflammatory factors and oxidative stress.ConclusionAS-IV enhanced the cell viability, and inhibited apoptosis, inflammation and oxidative stress of 6-OHDA-treated SH-SY5Y cells via activating the JAK2/STAT3 signaling pathway. This study may confer novel insights for the management of PD.

Verbal and nonverbal short-term memory impairment in untreated Parkinson's disease.

1993 ◽  
Vol 7 (3) ◽  
pp. 396-405 ◽  
Author(s):  
Edith V. Sullivan ◽  
Harvey J. Sagar ◽  
James A. Cooper ◽  
Nigel Jordan
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Memory Impairment ◽  
Short Term Memory ◽  
Short Term ◽  
Term Memory
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