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The Journal of Neuroscience, March 15, 1999, 19(6):1988-1997
Modification of Postsynaptic Densities after Transient Cerebral Ischemia: A Quantitative and Three-Dimensional Ultrastructural Study
Maryann E. Martone1, Ying Z. Jones1, Steve J. Young1, Mark H. Ellisman1, Justin A. Zivin1, and Bing-Ren Hu2 1 Department of Neurosciences, National Center for Microscopy and Imaging Research at San Diego, University of California, San Diego, La Jolla, California 92093, and 2 Center for the Study of Neurological Disease, Queen's Medical Center, Honolulu, Hawaii 92813
Abnormal synaptic transmission has been hypothesized to be a cause of neuronal death resulting from transient ischemia, although the mechanisms are not fully understood. Here, we present evidence that synapses are markedly modified in the hippocampus after transient cerebral ischemia. Using both conventional and high-voltage electron microscopy, we performed two- and three-dimensional analyses of synapses selectively stained with ethanolic phosphotungstic acid in the hippocampus of rats subjected to 15 min of ischemia followed by various periods of reperfusion. Postsynaptic densities (PSDs) from both area CA1 and the dentate gyrus were thicker and fluffier in postischemic hippocampus than in controls. Three-dimensional reconstructions of selectively stained PSDs created using electron tomography indicated that postsynaptic densities became more irregular and loosely configured in postischemic brains compared with those in controls. A quantitative study based on thin sections of the time course of PSD modification indicated that the increase in thickness was both greater and more long-lived in area CA1 than in dentate gyrus. Whereas the magnitude of morphological change in dentate gyrus peaked at 4 hr of reperfusion (140% of control values) and declined thereafter, changes in area CA1 persisted and increased at 24 hr of reperfusion (191% of control values). We hypothesize that the degenerative ultrastructural alteration of PSDs may produce a toxic signal such as a greater calcium influx, which is integrated from the thousands of excitatory synapses onto dendrites, and is propagated to the neuronal somata where it causes or contributes to neuronal damage during the postischemic phase.
Key words: postsynaptic density; hippocampus; cerebral ischemia; electron microscope; tomography; three-dimensional reconstruction; neuronal death
Copyright © 1999 Society for Neuroscience 0270-6474/99/1961988-10$05.00/0
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