| Project/Area Number |
60480259
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Psychiatric science
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| Research Institution | University of Tokyo |
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Principal Investigator |
KATO Takahiko University of Tokyo, Faculty of Medicine, 医学部, 助教授 (80010023)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAGUCHI Kazutyoshi University of Tokyo, Faculty of Medicine, 医学部, 助教授 (10009988)
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| Project Period (FY) |
1985 – 1987
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| Project Status |
Completed (Fiscal Year 1987)
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| Budget Amount *help |
¥6,500,000 (Direct Cost: ¥6,500,000)
Fiscal Year 1987: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1986: ¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 1985: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | Spinal motor neurons / Purkinje cells / Amacrine cells / Amyotrophic lateral sclerosis / Cerebellar layers / Retinal degeneration / Choline acetyltransferase / Glutamate decarboxylase / 背髄運動ニューロン / 単一ニューロン / グルタミン酸脱炭酸酵素 / GABA / 超微量分析 |
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| Research Abstract |
Freeze-dried sections of CNS tissues were prepared from control patients with non-neurological disease and patients with neurological diseases. Single neurons, as shown below, were isolated and microsamples of cerebellar layers and caudate nucleus were dissected out from these sections. Choline acetyltransferase (ChAT) and glutamate decarboxylase (GAD) activities and <gamma>-aminobutyric acid (GABA) concentration were assayed in these samples. GAD and GABA were analyzed in the retinas. from retinal-degeneration mice. (1) ALS motor neurons degenerate due to unknown etiology and atrophy to disappear at the far advanced stage. Many large cell bodies of motor neurons remained in the anterior horn of spinal cord section from non-advenced cases but a few atrophied and fragile cell bodies were detected with advanced cases. ChAT activity was far lower in the remaining large cell bodies than in control cell bodies. The activity became higher in the atrophied cell bodies with progress of patholo
… More
gical process. It was speculated that ChAT was produced much more in the atrophied cell bodies which supply ChAT to the many axon terminals sprouting to compensate innervation loss o fmuscle caused by cell degeneration. (2) Spinal motor neurons, a typical cholinergic neuron, contained GAD in animals and GABA was thought to be a kind of trophic factor to maintain the cell function and synaptic contact with muscle. Control numan motor neurons contain very low GAD activity. No change was observable in GAD activity of ALS motor neurons. (3) Human Purkinje cells from cerebellum had GAD activity much lower than those from rabbit and rat. Compared with animal samples, the activities were also lower in human caudate nucleus and in the molecular and granular layers from human cerebellum. These suggest that transmittersynthesyzing activity of human neuron is generally lower than that of animal neurons. (4) GABAergic amacrine cells of degenerating retinas contained markedly high levels of GAD activity and GABE concentration, compared with those in normal retina. GABA was thought to play a role as a trophic factor in response to degeneration process. Less
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