Modification of postsynaptic densities in neostriatum after transient ischemia.

CAPANI, F.; HU, B. R. ; GROVES, P. ; MARTONE, M. E.

New Orleans

Congreso; Society for Neuroscience Meeting; 2000

SFN

A 15 min episode of transient ischemia causes delayed neuronal death in the rat central nervous system. We have previously shown that a brief ischemic episode caused biochemical and neurodegenerative changes in post-synaptic densities (PSDs) in hippocampal area CA1 during the post-ischemic phase (Hu et al., 1998; Martone et al., 1999). Using selective staining with ethanolic phosphotungstic acid (E-PTA) and 2D and 3D electron microscopic analysis, PSDs exhibited a marked thickening of structure starting at 4 hours of reperfusion. In this study we employ the same technique to investigate PSD structure in the dorsal neostriatum, another brain area particularly vulnerable to ischemia. Rats brains subjected to 15 min. of ischemia followed by 1, 2, 6 and 24 hrs of reperfusion were stained with E-PTA and examined by electron microscopy. PSDs were noticeably thicker in postischemic tissue than in controls. A study of the time course indicated that the increase in PSD thickness started at 2 hours of reperfusion (128 % of the control values) and continued to increase up to 24 hr (193% of the control values). We conclude that PSDs in striatum are markedly modified and these modifications cause or contribute to neuronal damage during the postischemic period.