| Project/Area Number |
07671571
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Orthopaedic surgery
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| Research Institution | Chiba University |
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Principal Investigator |
MURAKAMI Masazumi Chiba University School of Medicine, Assistant, 医学部, 助手 (50219903)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1996: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1995: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | Motor-Evoked Potential / Hypoxia / Inhibitory Neurotransmitter / Interneuron / Glucose / 脊髄運動誘発電位 / in vitro頚髄標本 / シナプス伝達 / グルコース |
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| Research Abstract |
We studied the effects of hypoxia on synaptic transmission of motor pathway in spinal cord using in vitro preparations.
The cervical spinal cords of neonatal rats were isolated and superfused with oxygenated artificial cerebrospinal fluid (aCSF) at room temperature. The ventral root motor evoked potentials (VR-MEP) were recorded from C7 ventral roots in responce to stimulation to the ventrolateral funiculus (VLF) at Cl.
VR-MEP consisted of the early and the late components. The replacement of Ca^<2+> in aCSF by Mn^<2+> reversibly blocked both components supporting them to be trans-synaptic origin. Within 10-40 min of superfusion with hypoxic aCSF,the amplitudes of both components in VR-MEP increased to 130-140% of the control, and then declined progressively to 30% in 90 min. The latency of the early component was prolonged during hypoxia. After 60 min rexygenation, VR-MEP amplitudes recovered to 80-95% with full restoration of the latency.
The application of inhibitory amino acid antagonists strychnine (2muM) and picrotoxin (1muM) abolished the augmentation of VR-MEP amplitudes observed in the early phase of hypoxia. The present results suggested that in the early phase of hypoxia amplitudes of VR-MEP were increased because of selective depression of inhibitory synaptic transmission.
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