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大鼠垂体中的突触素免疫反应性:6-羟基多巴胺处理后的变化

Synaptophysin immunoreactivity in the rat pituitary: alterations after 6-hydroxydopamine treatment.

作者信息

Saland L C, Thomas D, Morales M, Gaddy J

机构信息

Department of Neurosciences, The University of New Mexico School of Medicine, Albuquerque 87131-5223, USA.

出版信息

Endocrine. 1998 Oct;9(2):201-6. doi: 10.1385/ENDO:9:2:201.

DOI:10.1385/ENDO:9:2:201
PMID:9867254
Abstract

Synaptophysin (SN) is a synaptic-vesicle-associated membrane protein whose presence is indicative of intact, functional synapses. This study examines the presence of SN in pituitary gland innervation after neurotoxin-induced denervation followed by reinnervation. Immunostaining of rat pituitary neurointermediate lobe tissue for SN reveals a pattern of dot-like densities in the intermediate lobe and intensely stained dispersed regions in the neural lobe of normal animals. In rats treated with 6-hydroxydopamine (6-OHDA), a catecholamine neurotoxin, by peripheral injection, there is a significant depletion of the SN immunostaining in the intermediate lobe, as well as a significant reduction of SN immunoreactivity in the neural lobe, in animals studied 1 wk after drug treatment, with computer analysis of the tissue sections. At 3 wk after 6-OHDA, there is a partial recovery of immunoreactivity for SN in the neural lobe in many tissue sections, and the intermediate lobe also contains only relatively sparse staining for the synaptic protein. Computer analysis revealed that at 3 wk after 6-OHDA, both lobes still had reduced SN immunoreactivity, but the difference in levels measured did not achieve statistical significance. These results contrast with the prior finding of significant recovery of immunoreactivity for GAP-43, a growth and regeneration-associated protein, in intermediate lobe innervation of rats treated with the same drug regimen. We suggest that 6-OHDA treatment damages synaptic vesicle integrity in both the intermediate and neural lobes of the pituitary, and that recovery is in progress, but not complete at 3 wk after the drug is administered.

摘要

突触素(SN)是一种与突触小泡相关的膜蛋白,其存在表明突触完整且功能正常。本研究检测了神经毒素诱导去神经支配后再支配的垂体神经支配中SN的存在情况。对大鼠垂体神经中间叶组织进行SN免疫染色,结果显示正常动物的中间叶有点状密度模式,神经叶有强烈染色的分散区域。通过外周注射儿茶酚胺神经毒素6-羟基多巴胺(6-OHDA)处理的大鼠,在药物处理后1周进行组织切片计算机分析,结果显示中间叶的SN免疫染色显著减少,神经叶的SN免疫反应性也显著降低。在6-OHDA处理后3周,许多组织切片中神经叶的SN免疫反应性部分恢复,中间叶对突触蛋白的染色也相对稀疏。计算机分析显示,在6-OHDA处理后3周,两个叶的SN免疫反应性仍然降低,但测量水平的差异未达到统计学意义。这些结果与先前在用相同药物方案处理的大鼠中间叶神经支配中生长和再生相关蛋白GAP-43免疫反应性显著恢复的发现形成对比。我们认为,6-OHDA处理会损害垂体中间叶和神经叶的突触小泡完整性,并且恢复正在进行,但在药物给药后3周尚未完成。

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本文引用的文献

1
GAP-43-Immunoreactive Nerve Fibers in the Rat Pituitary: Modulation after 6-Hydroxydopamine-Induced Degeneration and Regeneration.大鼠垂体中 GAP-43 免疫反应性神经纤维:6-羟多巴胺诱导退变和再生后的调节。
Mol Cell Neurosci. 1993 Dec;4(6):576-82. doi: 10.1006/mcne.1993.1071.
2
Degeneration and regeneration of nerve terminals in the rat pituitary pars intermedia after 6-hydroxydopamine treatment.6-羟多巴胺处理后大鼠垂体中间部神经末梢的退化和再生。
Mol Cell Neurosci. 1991 Oct;2(5):418-26. doi: 10.1016/1044-7431(91)90029-n.
3
Expression of synaptophysin in sprouting neurons after entorhinal lesion in the rat.
大鼠内嗅皮层损伤后新生神经元中突触素的表达
Exp Brain Res. 1997 Oct;117(1):80-6. doi: 10.1007/s002210050201.
4
Synaptophysin immunoreactivity in the aging rat pituitary gland.衰老大鼠垂体中的突触素免疫反应性
Brain Res Bull. 1997;43(6):561-4. doi: 10.1016/s0361-9230(97)80005-6.
5
Synaptophysin, a major synaptic vesicle protein, is not essential for neurotransmitter release.突触素是一种主要的突触小泡蛋白,对神经递质释放并非必不可少。
Proc Natl Acad Sci U S A. 1996 May 14;93(10):4760-4. doi: 10.1073/pnas.93.10.4760.
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Periventricular-hypophysial dopaminergic neurons innervate the intermediate but not the neural lobe of the rat pituitary gland.室周-垂体多巴胺能神经元支配大鼠垂体的中间叶而非神经叶。
Neuroendocrinology. 1995 Aug;62(2):147-54. doi: 10.1159/000126999.
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Differential distribution of synaptotagmin I and rab3 in the anterior pituitary of four mammalian species.四种哺乳动物垂体前叶中突触结合蛋白I和rab3的差异分布。
Neuroendocrinology. 1995 Aug;62(2):101-10. doi: 10.1159/000126994.
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Mice lacking synaptophysin reproduce and form typical synaptic vesicles.缺乏突触素的小鼠能够繁殖并形成典型的突触小泡。
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Dopamine transporter mRNA expression is intense in rat midbrain neurons and modest outside midbrain.
Brain Res Mol Brain Res. 1993 Apr;18(1-2):181-6. doi: 10.1016/0169-328x(93)90187-t.
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