Involvement of Astroglial Fibroblast Growth Factor-2 and Microglia in the Nigral 6-OHDA Parkinsonism and a Possible Role of Glucocorticoid Hormone on the Glial Mediated Local Trophism and Wound Repair

Silva, Camila; Fuxé, Kjell; Chadi, Gerson

doi:10.1007/978-3-211-92660-4_15

Cited by 10 publications

(12 citation statements)

References 84 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We also observed similar results with the immunohistochemistry assays for GFAP. Not only OX-42, but also GFAP immunoreactive cells were demonstrated in the 6-OHDA model [45, 46]. These authors showed that the OX-42 immunoreactivity increased in the substantia nigra , 2 h after the 6-OHDA injection, peaked at day 7 and remained increased in the 14th day.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Properties of a Standardized Extract fromMyracrodruon urundeuvaFr. All. (Aroeira-Do-Sertão), as Evaluated by a Parkinson’s Disease Model in Rats

Calou

Bandeira

Aguiar-Galvão

et al. 2014

Parkinson's Disease

View full text Add to dashboard Cite

Myracrodruon urundeuva Fr. All. (Anacardiaceae) is a Brazilian medicinal species, which is common to the Northeastern Brazilian semiarid region, whose stem-bark is widely used in folk medicine. It is an endangered species, presenting as main bioactive components tannins and chalcones. In this work, we studied the neuroprotective effects of a standardized extract from cultivated M. urundeuva (SEMU), in a model of Parkinson's disease. Thus, a unilateral injection of 6-OHDA was done into the rat right stratum. The animals were submitted to stereotaxic surgery, then treated with SEMU (5, 10, 20, or 40 mg/kg, p.o.) for 2 weeks, subjected to behavioral tests, and euthanized for striata dissections and neurochemical, histological, and immunohistochemical analyses. We showed, for the first time, that SEMU reverted behavioral alterations seen in the 6-OHDA-lesioned group and partially blocked the decrease in DA and DOPAC contents. The numbers of viable neurons and TH immunopositive cells were increased by SEMU. In addition, the SEMU-treated 6-OHDA groups showed lower numbers of GFAP and OX-42 immunopositive cells. The neuroprotective action of SEMU is possibly related to the antioxidant and anti-inflammatory properties of M. urundeuva, pointing out to its potential use in the prevention or treatment of neurodegenerative conditions, such as Parkinson's disease.

show abstract

Section: Discussionmentioning

confidence: 99%

Neuroprotective Properties of a Standardized Extract fromMyracrodruon urundeuvaFr. All. (Aroeira-Do-Sertão), as Evaluated by a Parkinson’s Disease Model in Rats

Calou

Bandeira

Aguiar-Galvão

et al. 2014

Parkinson's Disease

View full text Add to dashboard Cite

show abstract

“…FGF2 regulates dopaminergic neuron and nigrostriatal pathway development in vivo , the main pathway affected in humans in PD [11]. It has been shown that reactive astroglia display increased FGF2 immunoreactivity following dopaminergic cell degeneration induced by 6-hydroxydopamine (6-OHDA) lesions in the rat striatum, implying a possible mechanism of DAergic neuron repair [42]. Further evidence of the importance of FGF2 in dopaminergic neuron viability was shown by the finding that FGF2 enhances neuronal survivability and protects from 6-OHDA- induced cell death in the substantia nigra of PD mouse models [43].…”

Section: Fgf2 and Neurodegeneration: Therapeutic Innovationsmentioning

confidence: 99%

Fibroblast Growth Factor-2 Signaling in Neurogenesis and Neurodegeneration

Woodbury

Ikezu

2013

J Neuroimmune Pharmacol

209

156

View full text Add to dashboard Cite

Fibroblast growth factor-2 (FGF2), also known as basic FGF, is a multi-functional growth factor. One of the 22-member FGF family, it signals through receptor tyrosine kinases encoding FGFR1-4. FGF2 activates FGFRs in cooperation with heparin or heparin sulfate proteoglycan to induce its pleiotropic effects in different tissues and organs, which include potent angiogenic effects and important roles in the differentiation and function of the central nervous system (CNS). FGF2 is crucial to development of the CNS, which explains its importance in adult neurogenesis. During development, high levels of FGF2 are detected from neurulation onwards. Moreover, developmental expression of FGF2 and its receptors is temporally and spatially regulated, concurring with development of specific brain regions including the hippocampus and substantia nigra pars compacta. In adult neurogenesis, FGF2 has been implicated based on its expression and regulation of neural stem and progenitor cells in the neurogenic niches, the subventricular zone (SVZ) and the subgranular zone (SGZ) of the hippocampal dentate gyrus. FGFR1 signaling also modulates inflammatory signaling through the surface glycoprotein CD200, which regulates microglial activation. Because of its importance in adult neurogenesis and neuroinflammation, manipulation of FGF2/FGFR1 signaling has been a focus of therapeutic development for neurodegenerative disorders, such as Alzheimer’s disease, multiple sclerosis, Parkinson’s disease and traumatic brain injury. Novel strategies include intranasal administration of FGF2, administration of an NCAM-derived FGFR1 agonist, and chitosan-based nanoparticles for the delivery of FGF2 in pre-clinical animal models. In this review, we highlight current research towards therapeutic interventions targeting FGF2/FGFR1 in neurodegenerative disorders.

show abstract

“…The immune response after 6-OHDA lesion involves activated microglia, but also infiltration of other immune cells such as macrophages (Tentillier et al, 2016). Consequently, GC administration may promote neuroprotection through their well-documented anti-inflammatory effects (Silva et al, 2009; Tentillier et al, 2016). In addition, neurotrophic factor expression in striatum, including brain-derived neurotrophic factor, may also occur independently of GR-mediated mechanisms (Schulte-Herbruggen et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

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

Hao

Shabanpoor

Metz

2017

Neuroscience Letters

View full text Add to dashboard Cite

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.

show abstract

Involvement of Astroglial Fibroblast Growth Factor-2 and Microglia in the Nigral 6-OHDA Parkinsonism and a Possible Role of Glucocorticoid Hormone on the Glial Mediated Local Trophism and Wound Repair

Cited by 10 publications

References 84 publications

Neuroprotective Properties of a Standardized Extract fromMyracrodruon urundeuvaFr. All. (Aroeira-Do-Sertão), as Evaluated by a Parkinson’s Disease Model in Rats

Neuroprotective Properties of a Standardized Extract fromMyracrodruon urundeuvaFr. All. (Aroeira-Do-Sertão), as Evaluated by a Parkinson’s Disease Model in Rats

Fibroblast Growth Factor-2 Signaling in Neurogenesis and Neurodegeneration

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

Contact Info

Product

Resources

About