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去势对外源过氧化物酶掺入正中隆起“突触”小泡的影响。II. 雄性大鼠栅栏区的血管周围部分

Influence of castration on incorporation of exogenous peroxidase into "synaptic" vesicles of the median eminence. II. The perivascular part of the palisade zone in male rats.

作者信息

Stoeckart R, Jansen H G, Kreike A J

出版信息

Cell Tissue Res. 1975 May 27;159(1):11-21. doi: 10.1007/BF00231991.

DOI:10.1007/BF00231991
PMID:1097117
Abstract

In the median eminence of male rats, nerve profiles in the immediate vicinity of portal capillaries have been divided into 4 categories on the basis of their vesicular content: profiles a with agranular "synaptic" vesicles of about 50 nm, b with similar agranular vesicles and also with granular vesicles of mainly 60-140 nm, c with granular vesicles alone and d without vesicles. Twenty-four hours after castration, the percentage of profiles of category a was significantly increased when compared with sham-operated animals, whereas the percentage of profiles of category b was significantly decreased. After intravenous injection of exogenous peroxidase, especially the nerve profiles located in direct contact with the outer basement membrane of the portal capillaries contained peroxidase positive "synaptic" vesicles. Injection off peroxidase after castration resulted in a significant increase in the percentage of nerve profiles containing both peroxidase positive and peroxidase negative "synaptic" vesicles (category a). It is suggested that, in certain nerve terminals, castration may lead to release off the content of granular vesicles, which may contain gonadotropin releasing factor. This release then may cause that nerve terminals with agranular vesicles and granular vesicles (category b) change in their vesicular content and are therefore classified as terminals with only agranular vesicles (category a). An increased turnover rate in the ultrastructurally affected terminals may be reflected in increased uptake of exogenous peroxidase. The observations imply that certain neurones projecting to portal capillaries in the median eminence are, directly or indirectly, sensitive to changes in the level of gonadal steroids.

摘要

在雄性大鼠的正中隆起处,门静脉毛细血管紧邻区域的神经纤维根据其囊泡内容物被分为4类:a类纤维含有直径约50nm的无颗粒“突触”囊泡;b类纤维含有类似的无颗粒囊泡以及主要直径为60 - 140nm的颗粒囊泡;c类纤维仅含有颗粒囊泡;d类纤维不含囊泡。阉割24小时后,与假手术动物相比,a类纤维的百分比显著增加,而b类纤维的百分比显著降低。静脉注射外源性过氧化物酶后,尤其是与门静脉毛细血管外基底膜直接接触的神经纤维含有过氧化物酶阳性的“突触”囊泡。阉割后注射过氧化物酶导致同时含有过氧化物酶阳性和阴性“突触”囊泡的神经纤维(a类)百分比显著增加。有人提出,在某些神经末梢,阉割可能导致颗粒囊泡内容物的释放,颗粒囊泡可能含有促性腺激素释放因子。这种释放可能会使含有无颗粒囊泡和颗粒囊泡的神经末梢(b类)的囊泡内容物发生变化,因此被归类为仅含有无颗粒囊泡的末梢(a类)。超微结构受影响的末梢中周转率的增加可能反映在外源性过氧化物酶摄取的增加上。这些观察结果表明,投射到正中隆起门静脉毛细血管的某些神经元直接或间接地对性腺类固醇水平的变化敏感。

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Influence of castration on incorporation of exogenous peroxidase into "synaptic" vesicles of the median eminence. II. The perivascular part of the palisade zone in male rats.去势对外源过氧化物酶掺入正中隆起“突触”小泡的影响。II. 雄性大鼠栅栏区的血管周围部分
Cell Tissue Res. 1975 May 27;159(1):11-21. doi: 10.1007/BF00231991.
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Arch Histol Jpn. 1977;40 Suppl:303-15. doi: 10.1679/aohc1950.40.supplement_303.

本文引用的文献

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Ultrastructural changes in the nerve endings of the median eminence after nialamide-DOPA administration.给予尼亚酰胺-多巴后正中隆起神经末梢的超微结构变化。
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Ultrastructure of the median eminence of the rat.大鼠正中隆起的超微结构
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[Ultrastructure of the median eminence of the pigeon (Columba livia domestica) in various experimental conditions].[不同实验条件下家鸽(Columba livia domestica)正中隆起的超微结构]
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Endocrinology. 1971 Jun;88(6):1288-93. doi: 10.1210/endo-88-6-1288.
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Ultrastructural evidence for exocytosis in the median eminence of the rat.大鼠正中隆起处存在胞吐作用的超微结构证据。
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Evidence for a periodic release of LH in castrated male and female rats.
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Ultrastructure of the neurohaemal region of the toad median eminence.蟾蜍正中隆起神经血器官区域的超微结构。
Z Zellforsch Mikrosk Anat. 1969;93(2):182-212. doi: 10.1007/BF00336689.
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Some aspects of the interrelationship between central 5-hydroxytryptamine neurons and hormones.中枢5-羟色胺能神经元与激素之间相互关系的某些方面。
Adv Biochem Psychopharmacol. 1974;10:67-74.
10
Localization of tritiated dopamine in the median eminence of the rat hypothalamus by electron microscope autoradiography.用电子显微镜放射自显影法对大鼠下丘脑正中隆起中氚标记多巴胺进行定位。
Brain Res. 1973 Dec 7;63:474-8. doi: 10.1016/0006-8993(73)90127-3.