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Brain Arachidonic Acid Cascade Enzymes are Upregulated in a Rat Model of Unilateral Parkinson Disease

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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 D2-like receptor initiated AA hydrolysis from phospholipids by cytosolic phospholipase A2 (cPLA2) and subsequent metabolism by cyclooxygenase (COX)-2. In unilaterally 6-OHDA- and sham-lesioned rats, we measured brain expression of cPLA2, other PLA2 enzymes, and COX-2. Activity and protein levels of cPLA2 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 sPLA2 and Ca2+-independent iPLA2 expression did not differ between sides or groups. Thus, the tonically increased ipsilateral AA signal in the lesioned rat corresponds to upregulated cPLA2 and COX-2 expression within the AA metabolic cascade, which may contribute to symptoms and pathology in Parkinson disease.

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Abbreviations

AA:

Arachidonic acid

COX-2:

Cyclooxygenase-2

cPLA2 :

Cytosolic phospholipase A2

DAT:

Dopamine reuptake transporter

iPLA2 :

Calcium independent PLA2

NMDA:

N-methyl-d-aspartate

sPLA2 :

Secretory PLA2

5-HT:

5-hydroxytryptamine (serotonin)

6-OHDA:

6-hydroxydopamine

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Acknowledgments

This research was supported entirely by the Intramural Program of the National Institute on Aging.

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Correspondence to Abesh Kumar Bhattacharjee.

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Lee, HJ., Bazinet, R.P., Rapoport, S.I. et al. Brain Arachidonic Acid Cascade Enzymes are Upregulated in a Rat Model of Unilateral Parkinson Disease. Neurochem Res 35, 613–619 (2010). https://doi.org/10.1007/s11064-009-0106-6

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