IN-VIVO STUDIES OF EXTRACELLULAR METABOLITES IN THE STRIATUM AFTER DISTAL MIDDLE CEREBRAL-ARTERY OCCLUSION IN STROKE-PRONE SPONTANEOUSLY HYPERTENSIVE RATS
T. Shirotani et al., IN-VIVO STUDIES OF EXTRACELLULAR METABOLITES IN THE STRIATUM AFTER DISTAL MIDDLE CEREBRAL-ARTERY OCCLUSION IN STROKE-PRONE SPONTANEOUSLY HYPERTENSIVE RATS, Stroke, 26(5), 1995, pp. 878-884
Background and Purpose We demonstrated in a previous study that Ca-45
accumulation in the lateral part of the striatum was detected 3 days a
fter distal middle cerebral artery (MCA) occlusion using a Ca-45 autor
adiographic technique in stroke-prone spontaneously hypertensive rats.
However, the mechanism of delayed neuronal damage that occurred in th
e lateral part of the striatum is unknown. We examined changes in amin
o acids and monoamines in the striatums of rat brains after MCA occlus
ion in stroke-prone spontaneously hypertensive rats using an in vivo b
rain microdialysis technique. Methods Microdialysis probes were insert
ed into the lateral or medial part of the striatum 24 hours before the
experiment. The dialysis probe was perfused continuously at 2 mu L/mi
n with Ringer's solution, and the dialysate samples were collected eve
ry 20 minutes. After a 3-hour period for baseline stabilization, the r
ight MCA was occluded. The dialysate count of monoamines and amino aci
ds was determined by high-performance liquid chromatography. Results A
fter MCA occlusion, a threefold transient increase in glutamate was ob
served in the lateral part of the striatum. The level returned to its
baseline value 60 minutes after MCA occlusion. Dopamine in the lateral
part increased twofold to its peak value. This release persisted for
2 hours after MCA occlusion. There were no significant changes in thes
e components in the extracellular fluid of the medial part of. the str
iatum. Conclusions Our study demonstrated that changes of neurotransmi
tters in the lateral part of the striatum after MCA occlusion differed
from those in the medial part. These results suggest that excessive r
elease of glutamate and dopamine is related to delayed neuronal damage
that occurs in the lateral part of the striatum in this model.