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首页> 外文期刊>The European Journal of Neuroscience >Altered neuronal responses and regulation of neurotrophic proteins in the medial septum following fimbria-fornix transection in CNTF- and leukaemia inhibitory factor-deficient mice.
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Altered neuronal responses and regulation of neurotrophic proteins in the medial septum following fimbria-fornix transection in CNTF- and leukaemia inhibitory factor-deficient mice.

机译：在CNTF和白血病抑制因子缺乏小鼠中，经纤维-穹ni横断后，内侧中隔的神经元反应和神经营养蛋白的调节改变。

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Degeneration of axotomized GABAergic septohippocampal neurones has been shown to be enhanced in ciliary neurotrophic factor (CNTF)-deficient mice following fimbria-fornix transection (FFT), indicating a neuroprotective function of endogenous CNTF. Paradoxically, however, the cholinergic population of septohippocampal neurones was more resistant to axotomy in these mutants. As leukaemia inhibitory factor (LIF) has been identified as a potential neuroprotective factor for the cholinergic medial septum (MS) neurones, FFT-induced responses were compared in CNTF(-/-), LIF(-/-) and CNTF/LIF double knockout mice. In CNTF(-/-) mice, FFT-induced cholinergic degeneration was confirmed to be attenuated as compared with wildtype mice. The expression of both LIF and LIF receptor beta was increased in the MS providing a possible explanation for the enhanced neuronal resistance to FFT in these animals. However, ablation of the LIF gene also produced paradoxical effects; following FFT in LIF(-/-) mice no loss of GABAergic or cholinergic MS neurones was detectable during the first postlesional week, suggesting that other efficient neuroprotective mechanisms are activated in these animals. In fact, enhanced activation of astrocytes, a source of neurotrophic proteins, was indicated by increased up-regulation of glial fibrillary acidic protein and vimentin expression. In addition, mRNA levels for neurotrophin signalling components (e.g. nerve growth factor, p75(NTR)) were differentially regulated. The positive effect on axotomized cholinergic neurones seen in CNTF(-/-) and LIF(-/-) mice as well as the increased up-regulation of astrogliose markers was abolished in CNTF/LIF double knockout animals. Our results indicate that endogenous CNTF and LIF are involved in the regulation of neuronal survival following central nervous system lesion and are integrated into a network of neurotrophic signals that mutually influence their expression and function.
机译：已证明，在纤毛-穹ni横断（FFT）后，睫状神经营养因子（CNTF）缺陷型小鼠中，轴索化的GABA能海马海马神经元的变性得到增强，表明内源性CNTF的神经保护功能。然而，自相矛盾的是，在这些突变体中，海马间隔神经元的胆碱能种群对轴切术的抵抗力更大。由于白血病抑制因子（LIF）已被确定为胆碱能中隔（MS）神经元的潜在神经保护因子，因此在CNTF（-/-），LIF（-/-）和CNTF / LIF double中比较了FFT诱导的反应剔除小鼠。在CNTF（-/-）小鼠中，与野生型小鼠相比，证实FFT诱导的胆碱能变性减弱。 MS中LIF和LIF受体β的表达均增加，为这些动物对FFT的神经元抗性增强提供了可能的解释。但是，切除LIF基因也会产生矛盾的影响。在LIF（-/-）小鼠中进行FFT后，在病变后的第一周没有检测到GABA能或胆碱能MS神经元的丢失，这表明在这些动物中激活了其他有效的神经保护机制。实际上，神经胶质原纤维酸性蛋白和波形蛋白表达的上调增加表明星形胶质细胞是神经营养蛋白的来源，其活化增强。此外，神经营养蛋白信号成分（例如神经生长因子，p75（NTR））的mRNA水平受到差异调节。在CNTF / LIF双敲除动物中，取消了在CNTF（-/-）和LIF（-/-）小鼠中看到的对无轴索胆碱能神经元的积极作用以及星形胶质糖标记物的上调。我们的结果表明，内源性CNTF和LIF参与中枢神经系统病变后神经元存活的调节，并整合到相互影响其表达和功能的神经营养信号网络中。

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