Brain arachidonic acid cascade enzymes are upregulated in a rat model of unilateral parkinson disease

  • Lee H
  • Bazinet R
  • Rapoport S
 et al. 
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Abstract

Arachidonic acid (AA) signaling is upregulated in the caudate-putamen and frontal cortex of unilaterally 6-hydroxydopamine (6-OHDA) lesioned rats, a model for asymmetrical Parkinson disease. AA signaling can be coupled to D(2)-like receptor initiated AA hydrolysis from phospholipids by cytosolic phospholipase A(2) (cPLA(2)) and subsequent metabolism by cyclooxygenase (COX)-2. In unilaterally 6-OHDA- and sham-lesioned rats, we measured brain expression of cPLA(2), other PLA(2) enzymes, and COX-2. Activity and protein levels of cPLA(2) were significantly higher as was COX-2-protein in caudate-putamen, frontal cortex and remaining brain on the lesioned compared to intact side of the 6-OHDA lesioned rats, and compared to sham brain. Secretory sPLA(2) and Ca(2+)-independent iPLA(2) expression did not differ between sides or groups. Thus, the tonically increased ipsilateral AA signal in the lesioned rat corresponds to upregulated cPLA(2) and COX-2 expression within the AA metabolic cascade, which may contribute to symptoms and pathology in Parkinson disease.

Author-supplied keywords

  • 6-OHDA
  • Arachidonic acid
  • Asymmetry
  • Cascade
  • Cyclooxygenase-2
  • Cytosolic phospholipase A2
  • Dopamine
  • Parkinson disease
  • Rat
  • Signaling
  • Unilateral
  • Upregulation

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Authors

  • Ho Joo Lee

  • Richard P. Bazinet

  • Stanley I. Rapoport

  • Abesh Kumar Bhattacharjee

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