scholarly journals Minocycline Protects against Rotenone-Induced Neurotoxicity Correlating with Upregulation of Nurr1 in a Parkinson’s Disease Rat Model

2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
Congcong Sun ◽  
Yun Wang ◽  
Mingshu Mo ◽  
Chengyuan Song ◽  
Xingbang Wang ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Rat Model ◽  
Camp Response Element Binding ◽  
Motor Deficits ◽  
Camp Response Element ◽  
Protein Levels ◽  
Immobility Time ◽  
Element Binding Protein ◽  
Commercial Kits

The aim of this study was to investigate the effect of minocycline in rats with rotenone-induced Parkinson’s disease (PD). The open field test was performed to determine the motor ability of the rats. Double immunofluorescence staining was used to detect the expression of tyrosine hydroxylase (TH) and Nurr1 in the substantia nigra (SN) of rats. The relative protein levels of TH, Nurr1, and the total- and phosphorylated-cAMP-response element binding protein (CREB) were determined by western blot analysis. The production of reactive oxygen species (ROS) and nitric oxide (NO) was detected by commercial kits. After exposure to rotenone for 28 days, rats exhibited decreased ambulation and rearing frequency and prolonged immobility time with loss of TH positive neurons in the SN. The phosphorylation levels of CREB and Nurr1 expression decreased significantly accompanied with the release of ROS and NO. Minocycline alleviated the motor deficits of rats lesioned by rotenone and elevated the expression of TH, as well as suppressing the release of ROS and NO in the SN. That was in line with the elevated phosphorylation levels of CREB and Nurr1 expression. In conclusion, our present study showed minocycline protected against neurotoxicity in a rotenone-induced rat model of PD, which was correlated with upregulation of Nurr1.

Isolongifolene mitigates rotenone-induced dopamine depletion and motor deficits through anti-oxidative and anti-apoptotic effects in a rat model of Parkinson's disease

2021 ◽  
Vol 112 ◽  
pp. 101890
Author(s):  
Rengasamy Balakrishnan ◽  
Dhanraj Vijayraja ◽  
Thangavel Mohankumar ◽  
Dharmar Manimaran ◽  
Palanivel Ganesan ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Rat Model ◽  
Motor Deficits ◽  
Dopamine Depletion ◽  
Apoptotic Effects

scholarly journals Pharmacogenetic stimulation of cholinergic pedunculopontine neurons reverses motor deficits in a rat model of Parkinson’s disease

2015 ◽  
Vol 10 (1) ◽  
Author(s):  
Ilse S. Pienaar ◽  
Sarah E. Gartside ◽  
Puneet Sharma ◽  
Vincenzo De Paola ◽  
Sabine Gretenkord ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Rat Model ◽  
Motor Deficits ◽  
Stimulation Of

The effect of intra-striatal administration of GPR55 agonist (LPI) and antagonist (ML193) on sensorimotor and motor functions in a Parkinson’s disease rat model

2020 ◽  
pp. 1-7
Author(s):  
Iman Fatemi ◽  
Abbas Abdollahi ◽  
Ali Shamsizadeh ◽  
Mohammad Allahtavakoli ◽  
Ali Roohbakhsh
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Locomotor Activity ◽  
G Protein ◽  
Rat Model ◽  
Field Tests ◽  
Motor Deficits ◽  
G Protein Coupled Receptor ◽  
Motor Functions ◽  
G Protein Coupled

Abstract Objective: G protein-coupled receptor 55 (GPR55) is an orphan G protein-coupled receptor with various physiological functions. Recent evidence suggests that this receptor may be involved in the control of motor functions. Therefore, in the present study, we evaluated the effects of intra-striatal administration of GPR55 selective ligands in a rat model of Parkinson’s disease. Methods: Experimental Parkinson was induced by unilateral intra-striatal administration of 6-hydroxydopamine (6-OHDA, 10 µg/rat). L-α-lysophosphatidylinositol (LPI, 1 and 5 µg/rat), an endogenous GPR55 agonist, and ML193 (1 and 5 µg/rat), a selective GPR55 antagonist, were injected into the striatum of 6-OHDA-lesioned rats. Motor performance and balance skills were evaluated using the accelerating rotating rod and the ledged beam tests. The sensorimotor function of the forelimbs and locomotor activity were assessed by the adhesive removal and open field tests, respectively. Results: 6-OHDA-lesioned rats had impaired behaviours in all tests. Intra-striatal administration of LPI in 6-OHDA-lesioned rats increased time on the rotarod, decreased latency to remove the label, with no significant effect on slip steps, and locomotor activity. Intra-striatal administration of ML193 also increased time on the rotarod, decreased latency to remove the label and slip steps in 6-OHDA-lesioned rats mostly at the dose of 1 µg/rat. Conclusions: This study suggests that the striatal GPR55 is involved in the control of motor functions. However, considering the similar effects of GPR55 agonist and antagonist, it may be concluded that this receptor has a modulatory role in the control of motor deficits in an experimental model of Parkinson.

Electroacupuncture Restores Spatial Learning and Downregulates Phosphorylated N-Methyl-D-Aspartate Receptors in a Mouse Model of Parkinson's Disease

2017 ◽  
Vol 35 (2) ◽  
pp. 133-141 ◽  
Author(s):  
Kung-Wen Lu ◽  
Jun Yang ◽  
Ching-Liang Hsieh ◽  
Yu-Chan Hsu ◽  
Yi-Wen Lin
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Nmda Receptor ◽  
Protein Kinase ◽  
Spatial Learning ◽  
Long Term Potentiation ◽  
Camp Response Element Binding ◽  
Morris Water Maze Task ◽  
Element Binding Protein ◽  
6 Hydroxydopamine

Objective Parkinson's disease (PD) is a degenerative disorder of the central nervous system. PD can be classified as idiopathic, acquired or hereditary and may be caused by various factors such as oxidative stress, loss of mitochondrial function, neuronal excitotoxicity or calcium imbalance. Methods We hypothesised that electroacupuncture (EA) at KI3 would reduce neuronal excitotoxicity by regulating N-methyl-D-aspartate (NMDA) receptor function and may represent a novel therapeutic approach for PD. Results Our results showed that deficits in spatial learning (reflected by the escape latency time in the Morris water maze task) and long-term potentiation (LTP) caused by systemic 6-hydroxydopamine (6-OHDA) administration (that damages dopaminergic neurons) could be rescued by EA on day 3. In PD mice, phosphorylated NMDA receptor subunits NR1 and NR2B were elevated (134.03±10.17% and 123.46±3.47% of baseline levels, respectively) but total NR1 and NR2B was unaffected (101.37±3.87% and 102.61±4.22% of baseline, respectively). Elevated levels of pNR1 and pNR2B, and phosphorylated forms of protein kinase A, protein kinase C, α Ca2+/calmodulin-dependent protein kinase extracellular signal-regulated kinases (pERK), and cAMP response element-binding protein were also reduced following EA. Conclusions These novel findings suggest that EA can rescue learning and LTP deficits in a rodent model of PD. The results point to a possible role for EA-based approaches in the clinical treatment of learning deficits associated with PD.

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