A 6-Hydroxydopamine In Vivo Model of Parkinson’s Disease

Mercanti, Giulia; Bazzu, Gianfranco; Giusti, Pietro

doi:10.1007/978-1-61779-536-7_30

Cited by 22 publications

(10 citation statements)

References 17 publications

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“…This was the first report that addressed BBB opening and drug delivery in a PD model. Specifically, the authors used a neurotoxin-induced model of PD, which is characterized by a near complete acute destruction of the ipsilateral nigrostriatal pathway, hence emulating late-stage PD (26,27). One of the salient results of this study is the demonstration of motor improvements in 6-OHDA-leasioned rats following FUS-assisted transfection for GDNF.…”

Section: Introductionmentioning

confidence: 98%

Amelioration of the nigrostriatal pathway facilitated by ultrasound-mediated neurotrophic delivery in early Parkinson's disease

Karakatsani

Wang

Samiotaki

et al. 2019

Journal of Controlled Release

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The blood-brain barrier (BBB) prevents most drugs from gaining access to the brain parenchyma, which is a recognized impediment to the treatment of neurodegenerative disorders like Parkinson's disease (PD). Focused ultrasound (FUS), in conjunction with systemically administered microbubbles, opens the BBB locally, reversibly and non-invasively. Herein, we show that neither FUS applied over both the striatum and the ventral midbrain, without neurotrophic factors, nor intravenous administration of neurotrophic factors (either through protein or gene delivery) without FUS, ameliorates the damage to the nigrostriatal dopaminergic pathway in the sub-acute MPTP mouse model of early-stage PD. Conversely, the combination of FUS and intravenous

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Section: Introductionmentioning

confidence: 98%

Amelioration of the nigrostriatal pathway facilitated by ultrasound-mediated neurotrophic delivery in early Parkinson's disease

Karakatsani

Wang

Samiotaki

et al. 2019

Journal of Controlled Release

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“…The neurotoxic lesions of the nigrostriatal bundle were performed with injections of 6-hydroxydopamine hydrobromide (2 μl of 4 mg/ml in 0.9% saline with 0.02% ascorbic acid (Metz et al, 2001; Metz et al, 2005b) at the following coordinates: 4.0 mm posterior to bregma, 1.5 mm lateral to the midline, and 8.5 mm ventral to the skull surface, with the skull flat between lambda and bregma. The injection rate was set at 1 μl/min with 5 min allowed for diffusion (Paxinos and Watson, 1998, Mercanti et al, 2012). …”

Section: Methodsmentioning

confidence: 99%

Stress and corticosterone alter synaptic plasticity in a rat model of Parkinson’s disease

Hao

Shabanpoor

Metz

2017

Neuroscience Letters

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As a major influence on neuronal function and plasticity, chronic stress can affect the progression and symptoms of neurodegenerative conditions, such as Parkinson’s disease (PD). Here we investigated the influence of unilateral dopamine depletion and stress on dopamine-related hallmarks of stress response and neuronal plasticity in a rat model of PD. Animals received either restraint stress or a combination of adrenalectomy and corticosterone (CORT) supplementation to clamp circulating glucocorticoid levels for three weeks prior to unilateral nigrostriatal dopamine depletion. Rats were tested in skilled and gross motor function up to three weeks post-lesion. Midbrain mRNA expression assessments included markers of dopamine function and neuroplasticity, such as tyrosine hydroxylase (TH), synaptophysin (SYN), calcyon, and glucocorticoid receptor (GR). Along with impaired motor performance, stress and clamped CORT partially preserved TH expression in both substantia nigra (SN) and ventral tegmental area (VTA), but differentially modulated the expression of SYN, calcyon and GR mRNA in midbrain and cortical areas. Stress reduced synaptophysin mRNA expression in SN/VTA, and elevated calcyon mRNA optical density in both non-lesion and lesion hemispheres. Stress and CORT increased GR mRNA in the non-lesion SN/VTA, while in the lesion hemisphere GR mRNA was only elevated by CORT. In the motor cortex and striatum, however, GR was higher in both hemispheres under both experimental conditions. These findings suggest that stress and stress hormones differentially affect dopaminergic function and neuroplasticity in a rat model PD. The findings suggest a role for stress in motor and non-motor symptoms of PD and stress response.

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“…All surgeries were performed under sodium pentobarbital anesthesia, and all efforts were made to minimize suffering. e rat model was established by injecting 6-hydroxydopamine (6-OHDA) into the midbrain, according to the method used in a study [23]. Sprague Dawley (SD) male rats weighing 90-100 g were selected, anesthetized with 1% pentobarbital sodium, and fixed with a stereotaxic apparatus.…”

Section: Rat Model Of Parkinson's Diseasementioning

confidence: 99%

Plastrum Testudinis Extracts Promote NSC Differentiation into Dopaminergic Neuron by Regulating the Interaction of TET1 and FoxA2

Zhong

Zhou

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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In recent years, stem cells have gained much attention for the treatment of neurodegenerative diseases. However, inducing neural stem cell directionally differentiation is a difficult problem in the treatment of Parkinson's disease (PD) by stem cell therapy. Plastrum Testudinis (PT) can enhance the number of TH-positive neurons in the PD rat brain substantia nigra, but the underlying mechanism has not been clarified. Here, we aimed at further investigating the mechanism by which PT can promote NSC differentiation into dopaminergic neurons. A rat model of PD was used for detecting the effect of PT on the rat brain substantia nigra in vivo. e results showed the expressions of tyrosine hydroxylase (TH) and TET1 enzyme were increased after treatment with PT. Consequently, Plastrum Testudinis extracts (PTEs) were used for inducing NSC differentiation into dopaminergic neurons ex vivo. During differentiation of NSCs induced by PTE, TH expression was increased, with a concomitant increase in both TET1 and FoxA2. Next, we performed coimmunoprecipitation analysis to examine the interaction between TET1 protein and FoxA2 protein. Our results show that PTE can increase the binding rate of TET1 and FoxA2. us, our findings show that PTE can increase the efficiency of NSCs to directionally differentiate into dopaminergic neurons and provide experimental evidence for PT in the treatment of Parkinson's disease.

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A 6-Hydroxydopamine In Vivo Model of Parkinson’s Disease

Cited by 22 publications

References 17 publications

Amelioration of the nigrostriatal pathway facilitated by ultrasound-mediated neurotrophic delivery in early Parkinson's disease

Amelioration of the nigrostriatal pathway facilitated by ultrasound-mediated neurotrophic delivery in early Parkinson's disease

Stress and corticosterone alter synaptic plasticity in a rat model of Parkinson’s disease

Plastrum Testudinis Extracts Promote NSC Differentiation into Dopaminergic Neuron by Regulating the Interaction of TET1 and FoxA2

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