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妊娠期糖尿病导致出生后早期大鼠海马CA1和CA3亚区神经元丢失。

Gestational diabetes induced neuronal loss in CA1 and CA3 subfields of rat hippocampus in early postnatal life.

作者信息

Golalipour M J, Kafshgiri S Kaboli, Ghafari S

机构信息

Department of Anatomical Sciences, Gorgan Congenital Malformations Research Center, Gorgan, Iran.

出版信息

Folia Morphol (Warsz). 2012 May;71(2):71-7.

PMID:22648583
Abstract

This study was conducted to determine the effect of gestational diabetes on the neuronal density of CA1 and CA3 subfields of the hippocampus in Wistar rat offspring. On day 1 of gestation, 10 dams were randomly allocated into two control and diabetic groups. Five animals in the diabetic group received 40 mg/kg/b.w. of streptozotocin (intraperitoneally) and the control animals were received normal saline. Six offspring of each of the gestational diabetics and controls were randomly selected in postnatal days 7 and 21. The infants were scarified and coronal sections were taken from the right dorsal hippocampus and stained with cresyl violet. The number of pyramidal cells per 10000 μm(2) area and the thickness of layers of hippocampus in CA1 and CA3 were evaluated. In postnatal day 7, the number of pyramidal neurons in CA1 significantly reduced from 118.82 ± 8.0 in the control group to 84.71 ± 3.3 neurons in gestational diabetic group, and in postnatal day 21 it significantly reduced from 112.71 ± 6.9 in the control group to 91.52 ± 8.5 in the gestational diabetic group. Also, the number of pyramidal cells of CA3 on postnatal day 7 significantly reduced from 90.33 ± 8.1 in the control group to 62.86 ± 7.2 in the gestational diabetic group, and in P21 the number of pyramidal cells significantly reduced from 78.33 ± 2.4 in the control group to 61.7 ± 9.5 cells in the diabetic group. In CA1 and CA3 the thickness of the pyramidal layer on postnatal days 7 and 21 non-significantly increased in gestational diabetics in comparison with the controls. This study showed that uncontrolled gestational diabetes reduces the pyramidal neurons of the hippocampus in rat offspring.

摘要

本研究旨在确定妊娠期糖尿病对Wistar大鼠子代海马CA1和CA3亚区神经元密度的影响。在妊娠第1天,将10只母鼠随机分为两个对照组和糖尿病组。糖尿病组的5只动物接受40 mg/kg体重的链脲佐菌素(腹腔注射),对照组动物接受生理盐水。在出生后第7天和第21天,从每组妊娠期糖尿病母鼠和对照母鼠中随机选取6只子代。将幼鼠处死后,取右侧背侧海马的冠状切片,用甲酚紫染色。评估每10000μm²区域内锥体细胞的数量以及CA1和CA3区海马层的厚度。在出生后第7天,CA1区锥体细胞的数量从对照组的118.82±8.0显著减少至妊娠期糖尿病组的84.71±3.3个神经元;在出生后第21天,从对照组的112.71±6.9显著减少至妊娠期糖尿病组的91.52±8.5个神经元。此外,出生后第7天,CA3区锥体细胞的数量从对照组的90.33±8.1显著减少至妊娠期糖尿病组的62.86±7.2个;在出生后第21天,锥体细胞的数量从对照组的78.33±2.4显著减少至糖尿病组的61.7±9.5个。与对照组相比,在出生后第7天和第21天,妊娠期糖尿病母鼠子代CA1和CA3区锥体细胞层的厚度虽有增加,但无显著差异。本研究表明,未得到控制的妊娠期糖尿病会减少大鼠子代海马中的锥体细胞。

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