Sex differences in NeuN- and androgen receptor-positive cells in the bed nucleus of the stria terminalis are due to Bax-dependent cell death.
Sex differences in NeuN- and androgen receptor-positive cells in the bed nucleus of the stria terminalis are due to Bax-dependent cell death.
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DOI：
10.1016/j.neuroscience.2008.11.020
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发表时间：
2009-02-18
期刊：
影响因子：
3.3
通讯作者：
Forger, N. G.
中科院分区：
文献类型：
--
作者：
Holmes, M. M.;McCutcheon, J.;Forger, N. G.
一些物种的雄性终纹床核（BNSTp）的主核比雌性大。我们之前证明，在缺乏促死亡基因 bax 的小鼠中，BNSTp 细胞总数增加，细胞数量的性别差异被消除。这表明 Bax 依赖性细胞死亡是 BNSTp 性别分化的基础。然而，尚不清楚 BNSTp 中的哪些细胞受到 bax 缺失的影响。在这里，我们使用免疫组织化学和体视学技术来量化成年雄性和雌性 bax -/- 和 bax +/+ 小鼠 BNSTp 中表型鉴定的细胞。切片进行硫堇染色，或进行 NeuN 和 GFAP 双标记，以分别识别成熟神经元和星形胶质细胞；另一个系列被标记为雄激素受体（AR）。如前所述，在野生型小鼠中观察到 BNSTp 面积和细胞总数的性别差异，但在 bax -/- 动物中不存在。此外，野生型小鼠的 NeuN+ 和 AR+ 细胞数量存在性别差异（男性较多）。 Bax 基因缺失显着增加了 NeuN+ 和 AR+ 细胞的数量，并减少或消除了这些细胞类型的性别差异。 BNSTp 中的星形胶质细胞数量没有性别二态性，也不受 bax 基因状态的显着影响，尽管 bax -/- 小鼠中有更多 GFAP+ 细胞的趋势。与对照组相比，bax -/- 动物的总体脑重量也更大。我们得出的结论是，神经元和 AR+ 细胞数量的性别差异至少部分归因于 Bax 介导的细胞死亡。 bax -/- 小鼠中 NeuN+ 和 AR+ 细胞数量的增加表明，bax 敲除小鼠中的多余细胞与野生型小鼠中的细胞相似，并且保留了对雄激素做出反应的能力。
The principal nucleus of the bed nucleus of the stria terminalis (BNSTp) is larger in males than in females of several species. We previously demonstrated that in mice lacking the pro-death gene, bax, total BNSTp cell number is increased and sex differences in cell number are eliminated. This suggests that Bax-dependent cell death underlies sexual differentiation of the BNSTp. However, it is not known what cells in the BNSTp are affected by bax deletion. Here we used immunohistochemistry and stereological techniques to quantify phenotypically-identified cells in the BNSTp of adult male and female bax -/- and bax +/+ mice. Sections were thionin-stained, or double-labeled for NeuN and GFAP to identify mature neurons and astrocytes, respectively; an additional series was labeled for androgen receptor (AR). As previously demonstrated, sex differences in BNSTp area and overall cell number were seen in wildtype mice, but absent in bax -/- animals. In addition, sex differences (favoring males) were present in the number of NeuN+ and AR+ cells in wildtype mice. Bax gene deletion significantly increased the number of NeuN+ and AR+ cells and reduced or eliminated the sex differences in these cell types. The number of astrocytes in the BNSTp was not sexually dimorphic, nor significantly affected by bax gene status, although there was a trend for more GFAP+ cells in bax -/- mice. Overall brain weight was also greater in bax -/- animals compared to controls. We conclude that the sex differences in neuron and AR+ cell number are due at least in part to Bax-mediated cell death. Increased NeuN+ and AR+ cell number in bax -/- mice suggests that supernumerary cells in bax knockouts differentiate similarly to those in wildtype mice, and retain the capacity to respond to androgens.
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