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The Journal of Neuroscience, January 15, 1998, 18(2):625-633

Assembly of Proteins to Postsynaptic Densities after Transient Cerebral Ischemia

Bing-Ren Hu1, Minkyu Park2, Maryann E. Martone1, Wolfgang H. Fischer2, Mark H. Ellisman1, and Justin A. Zivin1

1 Department of Neuroscience, National Center for Microscopy and Imaging Research at San Diego, and Veterans Affairs Medical Center at San Diego, University of California, San Diego, La Jolla, California 92093-0624, and 2 The Clayton Foundation Laboratories for Peptide Biology, The Salk Institute, La Jolla, California 92037

Transient ischemia leads to changes in synaptic efficacy and results in selective neuronal damage during the postischemic phase, although the mechanisms are not fully understood. The protein composition and ultrastructure of postsynaptic densities (PSDs) were studied by using a rat transient ischemic model. We found that a brief ischemic episode induced a marked accumulation in PSDs of the protein assembly ATPases, N-ethylmaleimide-sensitive fusion protein, and heat-shock cognate protein-70 as well as the BDNF receptor (trkB) and protein kinases, as determined by protein microsequencing. The changes in PSD composition were accompanied by a 2.5-fold increase in the yield of PSD protein relative to controls. Biochemical modification of PSDs correlated well with an increase in PSD thickness observed in vivo by electron microscopy. We conclude that a brief ischemic episode modifies the molecular composition and ultrastructure of synapses by assembly of proteins to the postsynaptic density, which may underlie observed changes in synaptic function and selective neuronal damage.

Key words: postsynaptic density; synaptic plasticity; protein kinases; microsequencing; cerebral ischemia; electron microscope; neuronal damage

Copyright © 1998 Society for Neuroscience  0270-6474/98/182625-09$05.00/0


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