NMDA receptor antagonism potentiates the l-DOPA-induced extracellular dopamine release in the subthalamic nucleus of hemi-parkinson rats

Arfani, Anissa El; Bentea, Eduard; Aourz, Najat; Ampe, Ben; Deurwaerdère, Philippe De; Eeckhaut, Ann Van; Massie, Ann; Sarre, Sophie; Smolders, Ilse Julia; Michotte, Yvette

doi:10.1016/j.neuropharm.2014.05.024

Cited by 14 publications

(9 citation statements)

References 71 publications

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“…This reduction was reversed following treatment with SAFE or Madopar due to the restoration of the number of neurons. The λ in the 6-OHDA-induced rats treated with Madopar was slightly higher than that in the sham group, which is partially attributable to the fact that glutamate release induced by L-DOPA can also cause an increase in λ 20 52 53 . Furthermore, we found that was clearly decreased in the 6-OHDA-lesioned SN, due to the increase in astrogliosis and the potentially elevated levels of extracellular α-syn.…”

Section: Discussionmentioning

confidence: 86%

Neuroprotective Effects of A Standardized Flavonoid Extract of Safflower Against Neurotoxin-Induced Cellular and Animal Models of Parkinson’s Disease

Ren

Shi²,

Cao

et al. 2016

Sci Rep

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Safflower has long been used to treat cerebrovascular diseases in China. We previously reported that kaempferol derivatives of safflower can bind DJ-1, a protein associated with Parkinson's disease (PD), and flavonoid extract of safflower exhibited neuroprotective effects in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced mouse model of PD. In this study, a standardized safflower flavonoid extract (SAFE) was isolated from safflower and mainly contained flavonoids. Two marker compounds of SAFE, kaempferol 3-O-rutinoside and anhydrosafflor yellow B, were proven to suppress microtubule destabilization and decreased cell area, respectively. We confirmed that SAFE in dripping pill form could improve behavioural performances in a 6-hydroxydopamine (6-OHDA)-induced rat model of PD, partially via the suppression of α-synuclein overexpression or aggregation, as well as the suppression of reactive astrogliosis. Using an MRI tracer-based method, we found that 6-OHDA could change extracellular space (ECS) diffusion parameters, including a decrease in tortuosity and the rate constant of clearance and an increase in the elimination half-life of the tracer in the 6-OHDA-lesioned substantia nigra. SAFE treatment could partially inhibit the changes in ECS diffusion parameters, which might provide some information about neuronal loss and astrocyte activation. Consequently, our results indicate that SAFE is a potential therapeutic herbal product for treatment of PD.Parkinson's disease (PD) is the second most common disorder of the central nervous system (CNS), and its incidence is increasing among people over the age of 60 years 1 . PD is pathologically characterized by the loss of dopaminergic neurons in the substantia nigra (SN) and the formation of cytoplasmic inclusion bodies; however, the aetiology of PD remains elusive. The clinical features of PD include muscular rigidity, resting tremor, bradykinesia, and postural instability. By the time patients are diagnosed with PD, approximately 80% of the striatal dopamine terminals have been lost 2 , and destruction of terminal fields may precede cell body loss in the SN 3 . In rats, the unilateral intracerebral injection of 6-hydroxydopamine (6-OHDA) results in a selective degeneration of dopaminergic neurons, and this is a widely used animal model of PD. 6-OHDA induces a neurodegenerative process in the nigrostriatal system through the inhibition of mitochondrial complex function, which can lead to the induction of oxidative stress, inflammation 4-6 , abnormal protein aggregation 7,8 , elevated iron levels 9 and ultimately cell death. Dopamine replacement therapy remains the first line strategy in PD treatment. However, its effectiveness cannot modify the progression of the neurodegenerative process. Additionally, dopamine replacement therapy is associated with side-effects that include fluctuations in motor response and dyskinesia 10 . Increasing attention 1

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Section: Discussionmentioning

confidence: 86%

Neuroprotective Effects of A Standardized Flavonoid Extract of Safflower Against Neurotoxin-Induced Cellular and Animal Models of Parkinson’s Disease

Ren

Shi²,

Cao

et al. 2016

Sci Rep

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“…The total noradrenaline (NAD), dopamine (DA) and serotonin (5-HT) content as well as their metabolites 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA) and 5-hydroxyindolacetic acid (5-HIAA) in the striatum were measured based on previously reported methods 55 . In summary, after weighing striatal tissue, 190 µL of an antioxidant solution (0.1 M acetic acid, 3.3 mM L-cysteine, 0.27 mM Na2EDTA and 0.0125 mM ascorbic acid) and 10 µL of an internal standard solution (3,4-dihydroxybenzylamine solution 1 µg/mL in antioxidant) were added to the tissue.…”

Section: Methodsmentioning

confidence: 99%

Testosterone boosts physical activity in male mice via dopaminergic pathways

Jardí

Laurent

Kim

et al. 2018

Sci Rep

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Low testosterone (T) in men, especially its free fraction, has been associated with loss of energy. In accordance, orchidectomy (ORX) in rodents results in decreased physical activity. Still, the mechanisms through which T stimulates activity remain mostly obscure. Here, we studied voluntary wheel running behavior in three different mouse models of androgen deficiency: ORX, androgen receptor (AR) knock-out (ARKO) and sex hormone binding globulin (SHBG)-transgenic mice, a novel mouse model of “low free T”. Our results clearly show a fast and dramatic action of T stimulating wheel running, which is not explained by its action on muscle, as evidenced by neuromuscular studies and in a muscle-specific conditional ARKO mouse model. The action of T occurs via its free fraction, as shown by the results in SHBG-transgenic mice, and it implies both androgenic and estrogenic pathways. Both gene expression and functional studies indicate that T modulates the in vivo sensitivity to dopamine (DA) agonists. Furthermore, the restoration of wheel running by T is inhibited by treatment with DA antagonists. These findings reveal that the free fraction of T, both via AR and indirectly through aromatization into estrogens, stimulates physical activity behavior in male mice by acting on central DA pathways.

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“…This result is consistent with previous pathological studies. Arfani [ 14 ] reported that the increased extracellular STN DA level induced by long-term L-3,4-dihydroxyphenylalanine (L-DOPA) injection might result in dyskinesia and athetosis. Eberle-Wang demonstrated that injection of a 5-HT-like agonist in the subthalamic nucleus elicits orofacial dyskinesia in the rat [ 22 ].…”

Section: Discussionmentioning

confidence: 99%

“…The microdialysis study was carried out the next day. The progressive loading treadmill exercise protocol was modified from the Bedford treadmill exercise programme, and the loading was classified into 3 stages: stage I: 10 m · min -1 , 15 min; stage II: 15 m · min -1 , 15 min; stage III: 20 · min -1 , till exhaustion ( Figure 1 ) [ 14 ].…”

Section: Methodsmentioning

confidence: 99%

Increased extracellular dopamine and 5-hydroxytryptamine levels contribute to enhanced subthalamic nucleus neural activity during exhausting exercise

Liu

Qiao

2015

Biol Sport

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The purpose of the study was to explore the mechanism underlying the enhanced subthalamic nucleus (STN) neural activity during exhausting exercise from the perspective of monoamine neurotransmitters and changes of their corresponding receptors. Rats were randomly divided into microdialysis and immunohistochemistry study groups. For microdialysis study, extracellular fluid of the STN was continuously collected with a microdialysis probe before, during and 90 min after one bout of exhausting exercise. Dopamine (DA) and 5-hydroxytryptamine (5-HT) levels were subsequently detected with high-performance liquid chromatography (HPLC). For immunohistochemistry study, the expression of DRD2 and HT2C receptors in the STN, before, immediately after and 90 min after exhaustion was detected through immunohistochemistry technique. Microdialysis study results showed that the extracellular DA and 5-HT neurotransmitters increased significantly throughout the procedure of exhausting exercise and the recovery period (P<0.05 or P<0.01). Immunohistochemistry study results showed that the expression levels of DRD2 and HT2C in the rat STN immediately after exhausting exercise and at the time point of 90 min after exhaustion were both higher than those of the rest condition, but the difference was not significant (P>0.05). Our results suggest that the increased extracellular DA and 5-HT in the STN might be one important factor leading to the enhanced STN neural activity and the development of fatigue during exhausting exercise. This study may essentially offer useful evidence for better understanding of the mechanism of the central type of exercise-induced fatigue.

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NMDA receptor antagonism potentiates the l-DOPA-induced extracellular dopamine release in the subthalamic nucleus of hemi-parkinson rats

Cited by 14 publications

References 71 publications

Neuroprotective Effects of A Standardized Flavonoid Extract of Safflower Against Neurotoxin-Induced Cellular and Animal Models of Parkinson’s Disease

Neuroprotective Effects of A Standardized Flavonoid Extract of Safflower Against Neurotoxin-Induced Cellular and Animal Models of Parkinson’s Disease

Testosterone boosts physical activity in male mice via dopaminergic pathways

Increased extracellular dopamine and 5-hydroxytryptamine levels contribute to enhanced subthalamic nucleus neural activity during exhausting exercise

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