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大鼠纹状体中含神经降压素神经元的调节。喹啉酸和鹅膏蕈氨酸单侧纹状体损伤对神经降压素含量及其结合位点密度的影响。

Regulation of neurotensin-containing neurons in the rat striatum. Effects of unilateral striatal lesions with quinolinic acid and ibotenic acid on neurotensin content and its binding site density.

作者信息

Masuo Y, Montagne M N, Pélaprat D, Scherman D, Rostène W

机构信息

INSERM U.55, Hôpital Saint-Antoine, Paris, France.

出版信息

Brain Res. 1990 Jun 18;520(1-2):6-13. doi: 10.1016/0006-8993(90)91686-b.

DOI:10.1016/0006-8993(90)91686-b
PMID:2169955
Abstract

Recently, we reported bilateral increases in striatal neurotensin (NT) levels following unilateral 6-hydroxydopamine lesion of the nigrostriatal dopaminergic pathway. In the present study, the effect of unilateral striatal lesions with quinolinic acid (QA, 300 nmol) or ibotenic acid (IBO, 130 nmol) on striatal NT levels and binding site densities were analyzed in order to investigate other possible regulations of NT systems. QA and IBO injection decreased gamma-aminobutyric acid (GABA) levels and [125I]iodosulpride (a specific D2 receptor antagonist) binding site densities in the lesioned striatum, indicating degeneration of striatal intrinsic neurons. Striatal dopaminergic terminals were not altered by QA as shown by the lack of changes in [3H]dihydrotetrabenazine [( 3H]TBZOH, a specific ligand of the vesicular monoamine transporter) binding site densities. Moreover, QA lesion induced an increase in NT levels and a decrease in NT binding sites in the lesioned striatum without any change in the contralateral structure. In contrast to QA, IBO might destroy a certain proportion of dopaminergic terminals in the lesioned striatum, as shown by a 54% decrease in [3H]TBZOH binding. Furthermore, IBO lesion enhanced striatal NT levels bilaterally, while NT binding sites decreased in the lesioned striatum and increased in the contralateral side. The present results suggest that not only dopaminergic neurons but also striatal intrinsic neurons may control NT systems in the striatum.

摘要

最近,我们报道了黑质纹状体多巴胺能通路单侧6-羟基多巴胺损伤后纹状体神经降压素(NT)水平的双侧升高。在本研究中,分析了用喹啉酸(QA,300 nmol)或鹅膏蕈氨酸(IBO,130 nmol)进行单侧纹状体损伤对纹状体NT水平和结合位点密度的影响,以研究NT系统的其他可能调节机制。QA和IBO注射降低了损伤纹状体中γ-氨基丁酸(GABA)水平和[125I]碘舒必利(一种特异性D2受体拮抗剂)结合位点密度,表明纹状体内在神经元发生退变。[3H]二氢四苯嗪([3H]TBZOH,囊泡单胺转运体的特异性配体)结合位点密度未发生变化,表明QA未改变纹状体多巴胺能终末。此外,QA损伤导致损伤纹状体中NT水平升高和NT结合位点减少,而对侧结构无任何变化。与QA不同,IBO可能破坏了损伤纹状体中一定比例的多巴胺能终末,[3H]TBZOH结合减少54%即表明了这一点。此外,IBO损伤双侧增强了纹状体NT水平,而损伤纹状体中NT结合位点减少,对侧则增加。目前的结果表明,不仅多巴胺能神经元,而且纹状体内在神经元也可能控制纹状体中的NT系统。

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Regulation of neurotensin-containing neurons in the rat striatum. Effects of unilateral striatal lesions with quinolinic acid and ibotenic acid on neurotensin content and its binding site density.大鼠纹状体中含神经降压素神经元的调节。喹啉酸和鹅膏蕈氨酸单侧纹状体损伤对神经降压素含量及其结合位点密度的影响。
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引用本文的文献

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CNS Drugs. 2007;21(1):13-23. doi: 10.2165/00023210-200721010-00002.
2
The striatal neurotensin receptor modulates striatal and pallidal glutamate and GABA release: functional evidence for a pallidal glutamate-GABA interaction via the pallidal-subthalamic nucleus loop.纹状体神经降压素受体调节纹状体和苍白球谷氨酸及γ-氨基丁酸释放:通过苍白球-底丘脑核环路实现苍白球谷氨酸-γ-氨基丁酸相互作用的功能证据。
J Neurosci. 1998 Sep 1;18(17):6977-89. doi: 10.1523/JNEUROSCI.18-17-06977.1998.
3
High affinity neurotensin receptor mRNA distribution in rat brain and peripheral tissues. Analysis by quantitative RT-PCR.
大鼠脑和外周组织中高亲和力神经降压素受体mRNA的分布。定量逆转录聚合酶链反应分析。
J Mol Neurosci. 1997 Oct;9(2):93-102. doi: 10.1007/BF02736853.
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Turning behavior induced by intrastriatal injection of neurotensin in mice: sensitivity to non-peptide neurotensin antagonists.纹状体内注射神经降压素诱导小鼠的转向行为:对非肽类神经降压素拮抗剂的敏感性
Naunyn Schmiedebergs Arch Pharmacol. 1994 Jan;349(1):57-60. doi: 10.1007/BF00178206.