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Calpain activation in apoptosis of motoneurons in cell culture models of experimental parkinsonism.

Abstract
Parkinson's disease (PD) is a movement disorder characterized by progressive degeneration of primarily the dopaminergic neurons in the substantia nigra (SN). The present study briefly describes our findings to support the hypothesis that there is a possibility of degeneration of spinal cord (SC) motoneurons in course of parkinsonism. In cell culture models of experimental parkinsonism, we examined the degeneration of ventral SC motoneuron cell line (VSC4.1) following exposure to two different toxins, such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and rotenone. Our studies suggested calpain activation in the apoptosis of VSC4.1 motoneurons due to exposure to these parkinsonian toxins. Furthermore, our study showed the toxic effects of the dopaminergic toxin methamphetamine (METH) on VSC4.1 cells. The results strongly implicated a possible role for calpain in the mechanism of motoneuron apoptosis during parkinsonian degeneration, at large. Hence, we examined the neuroprotective efficacy of calpeptin, a specific inhibitor of calpain, in cell culture model of experimental parkinsonism.
AuthorsSupriti Samantaray, Swapan K Ray, Syed F Ali, Naren L Banik
JournalAnnals of the New York Academy of Sciences (Ann N Y Acad Sci) Vol. 1074 Pg. 349-56 (Aug 2006) ISSN: 0077-8923 [Print] United States
PMID17105932 (Publication Type: Evaluation Study, Journal Article)
Chemical References
  • Dipeptides
  • calpeptin
  • Calpain
Topics
  • Animals
  • Apoptosis
  • Calpain (antagonists & inhibitors, metabolism)
  • Cell Culture Techniques
  • DNA Fragmentation
  • Dipeptides (pharmacology)
  • Disease Models, Animal
  • Humans
  • In Situ Nick-End Labeling
  • Motor Neurons (drug effects, physiology)
  • Parkinsonian Disorders (therapy)
  • Rats

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