CHANGES IN NON-SYNAPTOSOMAL AND SYNAPTOSOMAL MITOCHONDRIAL MEMBRANE-LINKED ENZYMATIC-ACTIVITIES AFTER TRANSIENT CEREBRAL-ISCHEMIA

Citation
C. Cafe et al., CHANGES IN NON-SYNAPTOSOMAL AND SYNAPTOSOMAL MITOCHONDRIAL MEMBRANE-LINKED ENZYMATIC-ACTIVITIES AFTER TRANSIENT CEREBRAL-ISCHEMIA, Neurochemical research, 19(12), 1994, pp. 1551-1555
Citations number
19
Categorie Soggetti
Biology,Neurosciences
Journal title
ISSN journal
03643190
Volume
19
Issue
12
Year of publication
1994
Pages
1551 - 1555
Database
ISI
SICI code
0364-3190(1994)19:12<1551:CINASM>2.0.ZU;2-R
Abstract
Non-synaptosomal and synaptosomal mitochondrial membrane-linked enzyma tic activities, NADH-cytochromc c reductase rotenone insensitive (mark er of the outer membrane) and cytochrome oxidase (marker of the inner membrane), were measured in rat brain hippocampus and striatum immedia tely after and 1, 4, and 7 days following the induction of complete tr ansient ischemia (15 min) by the four vessel occlusion method. Further more citrate synthetase activity was measured with and without Triton X-100 in order to qualitatively evaluate the membrane permeability. No nsynaptosomal mitochondrial membranes showed reduction of both activit ies only in the late reperfusion phase: NADH-CCRRi decreased in striat al mitochondria after 4-7 days and only after 7 days in the hippocampu s. COX activity decreased only in striatal mitochondria 7 days after i schemia. Non-synaptosomal mitochondrial membrane permeability did not show changes. Synaptosomal mitochondria showed a decrease of NADH-CCRR i only at 7 days of reperfusion both in hippocampus and striatum, whil e COX activity decreased only during ischemia and returned to normal l evels in the following days in the two areas considered. In summary, f ree mitochondria showed insensitiveness to ischemia but they risulted damaged in the late reperfusion phase, while mitochondria from the syn aptic terminal showed ischemic damage, partially restored during reper fusion. The striatal mitochondria showed a major susceptibility to isc hemia/repefusion damage, showing changes earlier than the hippocampal ones.