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
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.