Degeneration of dopaminergic mesocortical neurons and activation of compensatory processes induced by a long-term paraquat administration in rats: Implications for Parkinson’s disease

@article{Ossowska2006DegenerationOD,
  title={Degeneration of dopaminergic mesocortical neurons and activation of compensatory processes induced by a long-term paraquat administration in rats: Implications for Parkinson’s disease},
  author={K. Ossowska and Maria Śmiałowska and Katarzyna Z Kuter and J. Wierońska and Barbara A. Zieba and Jadwiga Wardas and P. Nowak and Joanna Dabrowska and Aleksandra Bortel and Izabela Biedka and Gert Schulze and Hans Rommelspacher},
  journal={Neuroscience},
  year={2006},
  volume={141},
  pages={2155-2165}
}

Neonatal 6-hydroxydopamine lesioning of rats and dopaminergic neurotoxicity: proposed animal model of Parkinson’s disease

  • R. Kostrzewa
  • Biology, Psychology
    Journal of Neural Transmission
  • 2022
The n6-OHDA-lesioned rat is proposed as a PD model for its value in associating the SNpc dopaminergic lesion with behavioral outcomes, also for replicability of dopaminerg destruction, and the accompanying neuronal adaptations and interplay between neuronal phenotypes in brain—which provide a means to better define and understand the range of deficits and neuronal adaptations that are likely to occur in human PD.

Cyclooxygenase‐2 deficiency modifies the neurochemical effects, motor impairment and co‐morbid anxiety provoked by paraquat administration in mice

The results suggest that COX‐2 might differentially influence the motor and psychiatric symptoms associated with environmental toxin exposure, and indicate that the neurochemical impact of paraquat is not restricted to the nigrostriatal dopamine pathway but also involves stressor‐sensitive limbic regions.

The influence of preconditioning with low dose of LPS on paraquat-induced neurotoxicity, microglia activation and expression of α-synuclein and synphilin-1 in the dopaminergic system

Repeated, but small insults from oxidative stress and inflammation when administered in significant time intervals can counteract each other and even act protective as a preconditioning effect.

Glycogen Synthase Kinase 3β and Its Phosphorylated Form (Y216) in the Paraquat-Induced Model of Parkinsonism

The present data indicate that the long-term exposure of rats to PQ, a commonly used herbicide, diversely alters levels of GSK-3β in different brain structures, which may be associated with their vulnerability to its toxicity.

Alteration of GSK-3β in the hippocampus and other brain structures after chronic paraquat administration in rats.

The results of the present study indicate that PQ influenced levels and activation of GSK-3β in different brain structures, which may contribute to its toxicity, but on the other hand may suggest development of adaptive, protective mechanisms.
...

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The above results seem to suggest that long‐term paraquat administration produces a slowly progressing degeneration of nigrostriatal neurons, leading to delayed deficits in dopaminergic transmission, which may resemble early, presymptomatic, stages of Parkinson's disease.

Environmental Risk Factors and Parkinson's Disease: Selective Degeneration of Nigral Dopaminergic Neurons Caused by the Herbicide Paraquat

Findings unequivocally show that selective dopaminergic degeneration, one of the pathological hallmarks of PD, is also a characteristic of paraquat neurotoxicity.

Melanized dopaminergic neurons are differentially susceptible to degeneration in Parkinson's disease

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