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

  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},

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.



A slowly developing dysfunction of dopaminergic nigrostriatal neurons induced by long‐term paraquat administration in rats: an animal model of preclinical stages of Parkinson's disease?

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

Quantitative analysis of neuromelanin-pigmented neurons in control and parkinsonian midbrains demonstrates that the dopamine-containing cell groups of the normal human midbrain differ markedly from each other in the percentage of neurmelan in-pIGmented neurons they contain, and suggests a selective vulnerability of the neuromelsin- pigmented subpopulation of dopamine- containing mesencephalic neurons in Parkinson's disease.

Changes in dopaminergic neurons of the mesocorticolimbic system in Parkinson's disease.

The morphometric analysis performed on selected long-lasting 7 PD cases and 6 controls showed that cellular depletion in n.

The substantia nigra of the human brain. II. Patterns of loss of dopamine-containing neurons in Parkinson's disease.

The spatiotemporal progression of neuronal loss related to disease duration can be drawn in the substantia nigra pars compacta for each Parkinson's disease patient: depletion begins in the main pocket (nigrosome 1) and then spreads to other nigrosomes and the matrix along rostral, medial and dorsal axes of progression.

Mesocortical dopamine neurons. Lack of autoreceptors modulating dopamine synthesis.

Results suggest that transmitter synthesis in the prefrontal cortical terminals of mesocortical DA neurons is subject to end product inhibition and is regulated by changes in neuronal impulse flow, however, the synthesis of DA in these terminals does not seem to be modulated by DA autoreceptors.