Inhibition of tyrosine kinase receptor type B synthesis blocks axogenic effect of estradiol on rat hypothalamic neurones in vitro
Inhibition of tyrosine kinase receptor type B synthesis blocks axogenic effect of estradiol on rat hypothalamic neurones in vitro
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DOI：
10.1111/j.1460-9568.2004.03485.x
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发表时间：
2004-07-01
影响因子：
3.4
通讯作者：
Cambiasso, MJ
中科院分区：
文献类型：
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作者：
Brito, VI;Carrer, HF;Cambiasso, MJ
17-β-雌二醇（E2）促进离体雄性下丘脑神经元轴突生长和酪氨酸激酶受体（Trk）B水平。为了研究轴突反应是否依赖于TrkB的上调，我们分析了用针对TrkB mRNA的反义寡核苷酸处理的培养物中的神经炎生长和神经元极化。在没有E2的培养物中，用7.5或10 μ m反义处理降低了TrkB水平和显示可识别轴突的神经元的百分比;增加了小突起的数量和长度。在用5 μ m反义处理的培养物中，尽管总TrkB水平降低，但形态测量参数是正常的。相同的剂量阻止了TrkB水平的E2依赖性增加，并抑制了E2的轴突效应。这些结果表明，TrkB是必要的正常神经元的生长和成熟，并进一步表明，TrkB的增加是必要的E2发挥其轴向作用，在男性衍生的神经元。
17-pbeta-estradiol (E2) increases axonal growth and tyrosine kinase receptor (Trk)B levels of male-derived hypothalamic neurones in vitro. To investigate whether the axogenic response depends on the upregulation of TrkB, we analysed neuritic growth and neuronal polarization in cultures treated with an antisense oligonucleotide against TrkB mRNA. In cultures without E2, treatment with 7.5 or 10 mum antisense reduced TrkB levels and the percentage of neurones showing an identifiable axon; the number and length of minor processes were increased. In cultures treated with 5 mum antisense, morphometric parameters were normal although total TrkB levels were reduced. The same dose prevented the E2-dependent increase of TrkB levels and suppressed the axogenic effect of E2. These results indicate that TrkB is necessary for normal neuronal growth and maturation and further suggest that an increase in TrkB is necessary for E2 to exert its axogenic effect in male-derived neurones.