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

Neurochem Res. 2010 Apr;35(4):613-9. doi: 10.1007/s11064-009-0106-6. Epub 2009 Dec 8.


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.

Publication types

  • Research Support, N.I.H., Intramural

MeSH terms

  • Animals
  • Arachidonic Acid / metabolism*
  • Blotting, Western
  • Brain / enzymology*
  • Brain / metabolism
  • Cyclooxygenase 2 / metabolism*
  • Disease Models, Animal*
  • Male
  • Oxidopamine / pharmacology
  • Parkinson Disease / enzymology*
  • Parkinson Disease / metabolism
  • Phospholipases A2 / metabolism*
  • Rats
  • Rats, Inbred F344
  • Up-Regulation*


  • Arachidonic Acid
  • Oxidopamine
  • Cyclooxygenase 2
  • Phospholipases A2