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

Abstract Background: Parkinson's disease (PD) is a common neurodegenerative disorder characterized by progressive loss of nigrostriatal dopaminergic neurons leading to dopamine depletion and problems of movement, emotions and cognition. While the pathogenesis of PD is not clear, damage of dopaminergic neurons by oxygen-derived free radicals is considered an important contributing mechanism.This study aimed to evaluate the role of treadmill exercise in male Wister rats as a single treatment and as an aid-therapy with L-dopa for rotenone-induced PD. To study the role of NRF2-ARE pathway as a mechanism involved in exercise associated improvement in rotenone rat model of PD.Method: Animals were divided into 5 groups, (Control, rotenone, rotenone\exercise, rotenone\L-dopa, and rotenone\exercise\L-dopa (combination) groups). After the PD induction, rats in the rotenone\exercise and combination groups were daily treadmill exercised for 4 weeks.Results: Treadmill exercise significantly improved behavioral and motor aspects of rotenone model of PD. When treadmill exercise introduced as a single intervention, it amended most behavioral aspects of PD, gait fully corrected, short-term memory, and motor coordination. Where L-dopa corrected locomotor activity and motor co-ordination but failed to improve short-term memory and only partially corrected the gait of rotenone-treated rats. When treadmill exercise was combined with L-dopa, all features of PD were corrected. It was found that exercise upregulated some of its associative genes to NRF2 pathways such as TFAM, NRF2, Noq.1 mRNA expression.Conclusion: This study suggests that forced exercise improved parkinsonian like features by activating NRF2 pathway.

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Forced exercise activates the NrF2 pathway in the striatum and ameliorates motor and behavioral manifestations of Parkinson's disease in rotenone-treated rats

Behavioral and Brain Functions ◽

10.1186/s12993-020-00171-9 ◽

2020 ◽

Vol 16 (1) ◽

Author(s):

Dina M. Monir ◽

Motamed E. Mahmoud ◽

Omyma G. Ahmed ◽

Ibrahim F. Rehan ◽

Amany Abdelrahman

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Dopaminergic Neurons ◽

Motor Coordination ◽

Short Term Memory ◽

Treadmill Exercise ◽

Short Term ◽

Term Memory ◽

Nrf2 Pathway

Abstract Background Parkinson's disease (PD) is a common neurodegenerative disorder characterized by progressive loss of nigrostriatal dopaminergic neurons leading to dopamine depletion and problems of movement, emotions, and cognition. While the pathogenesis of PD is not clear, damage of dopaminergic neurons by oxygen-derived free radicals is considered an important contributing mechanism. This study aimed to evaluate the role of treadmill exercise in male Wister rats as a single treatment and as an aid-therapy with L-dopa for rotenone-induced PD. To study the role of the Nrf2- ARE pathway as a mechanism involved in exercise-associated improvement in rotenone-induced PD in rats. Method Animals were divided into 5 groups, (Control, rotenone, rotenone\exercise, rotenone\L-dopa, and rotenone\exercise\L-dopa (combination)groups). After the PD induction, rats in the rotenone\exercise and combination groups were daily treadmill exercised for 4 weeks. Results Treadmill exercise significantly improved behavioral and motor aspects of rotenone-induced PD. When treadmill exercise was introduced as a single intervention, it amended most behavioral aspects of PD, gait fully corrected, short-term memory, and motor coordination. Where L-dopa corrected locomotor activity and motor coordination but failed to improve short-term memory and only partially corrected the gait of rotenone-treated rats. When treadmill exercise was combined with L-dopa, all features of PD were corrected. It was found that exercise upregulated some of its associative genes to Nrf2 pathways such as TFAM, Nrf2 and NQO.1 mRNA expression. Conclusion This study suggests that forced exercise improved parkinsonian like features by activating the Nrf2 pathway.

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Different patterns of short-term memory deficit in Alzheimer's disease, Parkinson's disease and subjective cognitive impairment

Cortex ◽

10.1016/j.cortex.2020.06.016 ◽

2020 ◽

Vol 132 ◽

pp. 41-50

Author(s):

Nahid Zokaei ◽

Annie Sillence ◽

Annika Kienast ◽

Daniel Drew ◽

Olivia Plant ◽

...

Keyword(s):

Alzheimer’S Disease ◽

Parkinson’S Disease ◽

Alzheimer's Disease ◽

Parkinson's Disease ◽

Cognitive Impairment ◽

Short Term Memory ◽

Memory Deficit ◽

Short Term ◽

Term Memory ◽

Subjective Cognitive Impairment

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Lithium and valproate prevent olfactory discrimination and short-term memory impairments in the intranasal 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) rat model of Parkinson's disease

Behavioural Brain Research ◽

10.1016/j.bbr.2012.01.016 ◽

2012 ◽

Vol 229 (1) ◽

pp. 208-215 ◽

Cited By ~ 56

Author(s):

Adalberto A. Castro ◽

Karina Ghisoni ◽

Alexandra Latini ◽

João Quevedo ◽

Carla I. Tasca ◽

...

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Rat Model ◽

Short Term Memory ◽

Olfactory Discrimination ◽

Short Term ◽

Term Memory ◽

Memory Impairments

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

Open Life Sciences ◽

10.2478/s11535-008-0023-8 ◽

2008 ◽

Vol 3 (3) ◽

pp. 250-257 ◽

Cited By ~ 16

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.

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