| Project/Area Number |
05671173
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | KUMAMOTO UNIVERSITY MEDICAL SCHOOL |
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Principal Investigator |
NAGAHIRO Shinjl KUMAMOTO UNIVERSITY HOSPITAL DEPARTMENT OF NEUROSURGERY,LECTURER, 医学部・附属病院, 講師 (60145315)
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| Co-Investigator(Kenkyū-buntansha) |
GOTO Satoshi KUMAMOTO UNIVERSITY HOSPITAL DEPARTMENT OF NEUROSURGERY,LECTURER, 医学部・附属病院, 講師 (50240916)
USHIO Yukitaka KUMAMOTO UNIVERSITY MEDICAL SCHOOL DEPARTMENT OF NEUROSURGERY,PROFESSOR, 医学部, 教授 (20028583)
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| Project Period (FY) |
1993 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1995: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1994: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1993: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | TRANSIENT CEREBRAL ISCHEMIA / STRIATUM / SUBSTANTIA NIGRA / MAGNETIC RESONANCE IMAGING / APOMORPHINE / MICROGLIA / IMMUNOHISTOCHEMISTRY / TRANSPLANTATION / カルレチニン / 燐酸化チロシン / ミクログリア / 移植 / 再生 / 免疫組織化学 / カルシウム結合蛋白 / 一過性虚所脳虚血 / 脳血管透過性 / アポモルフィン / カルシニューリン |
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| Research Abstract |
Behavioral, magnetic resonance imaging and histological studies were performed on the striatonigral system of rats with unilateral reversible middle cerebral occlusion, and following results were obtained.
(1) The rats subjected to 15 to 120 minutes ischemia exhibited the ipsiversive rotational behavior elicited by systemic administration of dopamine receptor agonist apomorphine.
(2) magnetic resonance imaging study showed that T2 high-signal-intensity aresa appeared earlier in the ipsilateral striatum and cortex and the size increased with the duration of ischemia. Disruption of the blood-cerebrospinal fluid barrier following transient ischemia was demonstrated by MR imaging using Gd-DTPA enhancement.
(3) Histologically, the ipsilateral striatum of the rats showed a subdivisional ischemic injury. The striatal lesions having a cell type-specific injury were located in the dorsolateral portion of the rostral striatum. There was also a marked depletion of striatonigral afferents in the lateral portion of the substantia nigra pars reticulata. Activation of the microglia was noted in the ipsilateral cortex and the substantia nigra following ischemia.
(4) Immunohistochemical study in the rat with striatal ischemic lesion followed by intrastriatal grafts derived from fetal striatal peimordia demonstrated that the striatopallidal pathway was reformend by striatal projection neurons of the transplants.
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