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First published online 19 August 2008
doi: 10.1242/jcs.032987

Journal of Cell Science 121, 3015-3024 (2008)
Published by The Company of Biologists 2008
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Research Article

Cytosolic PLA2{alpha} activation in Purkinje neurons and its role in AMPA-receptor trafficking

Masato Mashimo1, Tetsuya Hirabayashi1,2,*, Toshihiko Murayama1 and Takao Shimizu3

1 Laboratory of Chemical Pharmacology, Graduate School of Pharmaceutical Sciences, Chiba University, Chuo-ku, Chiba 260-8675, Japan
2 Biomembrane Signaling Project, The Tokyo Metropolitan Institute of Medical Science, Bunkyo-ku, Tokyo 113-8613, Japan
3 Department of Biochemistry and Molecular Biology, Faculty of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo 113-0033, Japan

* Author for correspondence (e-mail: hirabayashi-tt{at}igakuken.org.jp)

Accepted 18 June 2008

Cytosolic phospholipase A2{alpha} (cPLA2{alpha}) selectively releases arachidonic acid from membrane phospholipids and has been proposed to be involved in the induction of long-term depression (LTD), a form of synaptic plasticity in the cerebellum. This enzyme requires two events for its full activation: Ca2+-dependent translocation from the cytosol to organelle membranes in order to access phospholipids as substrates, and phosphorylation by several kinases. However, the subcellular distribution and activation of cPLA2{alpha} in Purkinje cells and the role of arachidonic acid in cerebellar LTD have not been fully elucidated. In cultured Purkinje cells, stimulation of AMPA receptors, but not metabotropic glutamate receptors, triggered translocation of cPLA2{alpha} to the somatic and dendritic Golgi compartments. This translocation required Ca2+ influx through P-type Ca2+ channels. AMPA plus PMA, a chemical method for inducing LTD, released arachidonic acid via phosphorylation of cPLA2{alpha}. AMPA plus PMA induced a decrease in surface GluR2 for more than 2 hours. Interestingly, this reduction was occluded by a cPLA2{alpha}-specific inhibitor. Furthermore, PMA plus arachidonic acid caused the prolonged internalization of GluR2 without activating AMPA receptors. These results suggest that cPLA2{alpha} regulates the persistent decrease in the expression of AMPA receptors, underscoring the role of cPLA2{alpha} in cerebellar LTD.

Key words: cPLA2{alpha}, Purkinje neuron, LTD, Translocation, AMPA receptor, Ca2+


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