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帕金森病患者脑脊液中γ-氨基丁酸水平较低。左旋多巴和卡比多巴的作用。

Low CSF gamma-aminobutyric acid levels in Parkinson's Disease. Effect of levodopa and carbidopa.

作者信息

Manyam B V

出版信息

Arch Neurol. 1982 Jul;39(7):391-2. doi: 10.1001/archneur.1982.00510190009002.

Abstract

Levels of gamma-aminobutyric acid (GABA) in CSF were measured in patients with Parkinson's disease (n = 14) and sex-matched controls (n = 14). One patient underwent a spinal tap before and after treatment. The mean (+/- SD) CSF GABA levels were 200 +/- 70 pmole/mL in controls and 121 +/- 52 pmole/mL in patients with Parkinson's disease. In the untreated patients with Parkinson's disease, the CSF GABA level was 95 +/- 31 pmole/mL (n = 7) and in those who were treated with levodopa and carbidopa the level was 144 +/- 53 pmole/mL (n = 8). No significant difference was seen in plasma GABA levels between the controls and patients with Parkinson's disease. The decreased GABA level in CSF, which was elevated by levodopa, supports the concept that in Parkinson's disease, the GABA-dopamine interaction in the substantia nigra may be an important compensatory mechanism counteracting the dopamine neuronal loss.

摘要

对14例帕金森病患者和14例性别匹配的对照者测量了脑脊液中γ-氨基丁酸(GABA)的水平。1例患者在治疗前后接受了腰椎穿刺。对照组脑脊液GABA的平均(±标准差)水平为200±70皮摩尔/毫升,帕金森病患者为121±52皮摩尔/毫升。在未经治疗的帕金森病患者中,脑脊液GABA水平为95±31皮摩尔/毫升(n = 7),在接受左旋多巴和卡比多巴治疗的患者中,该水平为144±53皮摩尔/毫升(n = 8)。对照组和帕金森病患者的血浆GABA水平未见显著差异。脑脊液中降低的GABA水平被左旋多巴升高,这支持了以下观点:在帕金森病中,黑质中的GABA-多巴胺相互作用可能是一种重要的代偿机制,可抵消多巴胺神经元的损失。

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