Cell and Tissue Research

, Volume 350, Issue 3, pp 401–407

Physical activity is linked to ceruloplasmin in the striatum of intact but not MPTP-treated primates

  • Rehana K. Leak
  • Krassimira A. Garbett
  • Amanda M. Dettmer
  • Zhiming Zhang
  • Károly Mirnics
  • Judy L. Cameron
Short Communication

DOI: 10.1007/s00441-012-1488-3

Cite this article as:
Leak, R.K., Garbett, K.A., Dettmer, A.M. et al. Cell Tissue Res (2012) 350: 401. doi:10.1007/s00441-012-1488-3

Abstract

Ceruloplasmin is a protective ferroxidase. Although some studies suggest that plasma ceruloplasmin levels are raised by exercise, the impact of exercise on brain ceruloplasmin is unknown. We have examined whether striatal ceruloplasmin is raised with treadmill exercise and/or is correlated with spontaneous physical activity in rhesus monkeys. Parkinson’s disease is characterized by a loss in ceruloplasmin and, similarly, Parkinson’s models lead to a loss in antioxidant defenses. Exercise might protect against Parkinson’s disease and is known to prevent antioxidant loss in experimental models. We have therefore examined whether treadmill exercise prevents ceruloplasmin loss in monkeys treated unilaterally with the dopaminergic neurotoxin MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine). We found that exercise raised ceruloplasmin expression in the caudate and accumbens but not the putamen of intact monkeys. However, putamen ceruloplasmin was correlated with spontaneous activity in a home pen. MPTP alone did not cause unilateral loss of ceruloplasmin but blocked the impact of exercise on ceruloplasmin. Similarly, the correlation between putamen ceruloplasmin and activity was also lost with MPTP. MPTP elicited loss of tyrosine hydroxylase in the treated hemisphere; the remaining tyrosine hydroxylase was correlated with overall daily activity (spontaneous activity plus that induced by the treadmill). Thus, treadmill activity can raise ceruloplasmin but this impact and the link with spontaneous activity are both diminished in Parkinsonian primates. Furthermore, low overall physical activity predicts greater loss of dopaminergic phenotype in MPTP-treated primates. These data have implications for the maintenance of active lifestyles in both healthy and neurodegenerative conditions.

Keywords

Parkinson’s disease Neurodegeneration Antioxidant Exercise MPTP Rhesus monkey (female) 

Copyright information

© Springer-Verlag 2012

Authors and Affiliations

  • Rehana K. Leak
    • 1
    • 7
  • Krassimira A. Garbett
    • 2
    • 3
  • Amanda M. Dettmer
    • 4
  • Zhiming Zhang
    • 5
    • 6
  • Károly Mirnics
    • 2
    • 3
  • Judy L. Cameron
    • 4
  1. 1.Division of Pharmaceutical Sciences, Mylan School of PharmacyDuquesne UniversityPittsburghUSA
  2. 2.Department of PsychiatryVanderbilt UniversityNashvilleUSA
  3. 3.Vanderbilt Kennedy Center for Research on Human DevelopmentVanderbilt UniversityNashvilleUSA
  4. 4.Department of PsychiatryUniversity of PittsburghPittsburghUSA
  5. 5.Department of Anatomy & Neurobiology, College of MedicineUniversity of KentuckyLexingtonUSA
  6. 6.Morris K. Udall Parkinson’s Disease Research Center for Excellence, College of MedicineUniversity of KentuckyLexingtonUSA
  7. 7.Division of Pharmaceutical SciencesDuquesne UniversityPittsburghUSA

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