Reduction of 3-Methoxytyramine Concentrations in the Caudate Nucleus of Rats after Exposure to High-Energy Iron Particles: Evidence for Deficits in Dopaminergic Neurons

1990 ◽  
Vol 121 (2) ◽  
pp. 169 ◽  
Author(s):  
Walter A. Hunt ◽  
Thomas K. Dalton ◽  
James A. Joseph ◽  
Bernard M. Rabin
Keyword(s):  
Caudate Nucleus ◽  
Dopaminergic Neurons ◽  
High Energy ◽  
Iron Particles

Surface modification of iron particles with polystyrene and surfactants under high-energy ball milling

2013 ◽  
Vol 236 ◽  
pp. 429-437 ◽  
Author(s):  
Alexander V. Syugaev ◽  
Alena N. Maratkanova ◽  
Anatoly A. Shakov ◽  
Alexander V. Nelyubov ◽  
Svetlana F. Lomayeva
Keyword(s):  
Surface Modification ◽  
Ball Milling ◽  
High Energy ◽  
High Energy Ball Milling ◽  
Iron Particles ◽  
Energy Ball

Genotoxic Effects of High-Energy Iron Particles in Human Lymphoblasts Differing in Radiation Sensitivity

2001 ◽  
Vol 156 (2) ◽  
pp. 186-194 ◽  
Author(s):  
H. H. Evans ◽  
M-F. Horng ◽  
Thomas E. Evans ◽  
R. Jordan ◽  
J. L. Schwartz
Keyword(s):  
Radiation Sensitivity ◽  
High Energy ◽  
Iron Particles ◽  
Genotoxic Effects

Behavioral and neurochemical abnormalities after exposure to low doses of high-energy iron particles

1989 ◽  
Vol 9 (10) ◽  
pp. 333-336 ◽  
Author(s):  
Walter A. Hunt ◽  
James A. Joseph ◽  
Bernard M. Rabin
Keyword(s):  
High Energy ◽  
Low Doses ◽  
Iron Particles

Intrastriatal implantation of interleukin-1

1994 ◽  
Vol 80 (3) ◽  
pp. 484-490 ◽  
Author(s):  
Jin Wang ◽  
Krzysztof S. Bankiewicz ◽  
Robert J. Plunkett ◽  
Edward H. Oldfield
Keyword(s):  
Substantia Nigra ◽  
Caudate Nucleus ◽  
Ventral Tegmental Area ◽  
Dopaminergic Neurons ◽  
Interleukin 1 ◽  
Behavioral Recovery ◽  
Content Type ◽  
Median Forebrain Bundle ◽  
Ventral Tegmental ◽  
Fine Print

✓ Intrastriatal implantation with dopaminergic or nondopaminergic tissue can elicit behavioral recovery in parkinsonian animals. Because in these animals, especially in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned monkeys, there are still considerable numbers of dopaminergic neurons left in the mesencephalon, implantation-induced trophic effects on host residual dopaminergic neurons have been suggested as a mechanism underlying the behavioral recovery. Gliosis around the graft is a universal finding in any implantation procedure and is probably mediated by interleukin-1 (IL-1); in addition, activated astrocytes secrete several neurotrophic factors in vitro. Therefore, the authors postulated that trophic effects from IL-1-induced gliosis may be a “final common pathway” for recovery in parkinsonian animals after implantation. Hemiparkinsonism was induced in rats by injection of 6-hydroxydopamine either directly into the substantia nigra or into the median forebrain bundle. The substantia nigra-lesioned rats showed complete depletion of dopaminergic neurons in the substantia nigra but sparing of those in the ventral tegmental area, whereas the median forebrain bundle-lesioned animals had depletion of dopaminergic cells in the substantia nigra and the ventral tegmental area. Polymer pellets containing either slow-released IL-1 alpha and beta or placebo pellets were implanted in the caudate nucleus on the lesioned side in both groups. The rats' rotational response to amphetamine was tested weekly for 8 weeks. Selective substantia nigra-lesioned rats with implantation of IL-1 pellets had a 45% reduction in amphetamine-induced rotation, whereas placebo-implanted substantia nigra-lesioned rats had a 14% reduction in rotation. In the median forebrain bundle-lesioned group, neither IL-1 nor placebo implantation elicited any effect on turning. Immunohistochemical staining for glial fibrillary acidic protein was markedly increased surrounding the IL-1 pellets compared to the placebo pellets. In the selective substantia nigra-lesioned rats with IL-1 pellets implanted in the caudate nucleus, a considerable number of tyrosine hydroxylase immunoreactive (TH-IR) fibers were observed in the medial and middle portions of the caudate nucleus. Fewer TH-IR fibers were seen in the rats with placebo-bearing pellets. These results suggest that neurotrophic activities mediated by IL-1 and reactive astrocytes might be a common path through which tissue trauma and some tissue transplants exert their beneficial effects in parkinsonian animals. Furthermore, most of the sprouted dopaminergic fibers induced by IL-1 in the caudate nucleus come from dopaminergic neurons in the ventral tegmental area.

An Assessment of the Behavioral Toxicity of High-Energy Iron Particles Compared to Other Qualities of Radiation

1989 ◽  
Vol 119 (1) ◽  
pp. 113 ◽  
Author(s):  
Bernard M. Rabin ◽  
Walter A. Hunt ◽  
James A. Joseph
Keyword(s):  
High Energy ◽  
Iron Particles ◽  
Behavioral Toxicity

Neuroinflammation caused by activated microglia and astrocytes can contribute to the progression of pathogenic damage to substantia nigra neurons, playing a role in Parkinson's disease progression

2021 ◽  
Author(s):  
Moataz Dowaidar
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Substantia Nigra ◽  
Mitochondrial Dysfunction ◽  
Dopaminergic Neurons ◽  
Molecular Mechanisms ◽  
High Energy ◽  
Molecular Pathways ◽  
Activated Microglia

Parkinson's disease progresses by a number of regionally specific cellular and molecular mechanisms. Furthermore, these pathways interact and have an influence on one another in both normal and pathological conditions. Neuroinflammation caused by activated microglia and astrocytes can contribute to the progression of pathogenic damage to substantia nigra (SN) neurons. Similarly, oxidative stress may be caused by a variety of stressors, such as contaminants in the environment or age-related mitochondrial dysfunction, leading to the production of reactive oxygen species (ROS). Dopamine auto-oxidation is a significant generator of ROS in dopaminergic neurons, resulting in neuronal oxidative stress. The high energy demands of dopaminergic neurons may result in mitochondrial dysfunction and oxidative damage as they age. Because mitophagy clears dysfunctional mitochondria from SN neurons, mutation-related abnormalities in autophagy of defective proteins might allow damaging proteins to accumulate in the cell. Because the effects of aging on these molecular pathways and cellular activities are unknown, further study into these molecular pathways and their connections in normal and sick states will be essential for developing disease-specific therapies.

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