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白血病抑制因子对小鼠轴突切断后初级感觉神经元中甘丙肽/GMAP和神经肽Y表达的影响。

Influence of leukemia inhibitory factor on galanin/GMAP and neuropeptide Y expression in mouse primary sensory neurons after axotomy.

作者信息

Corness J, Shi T J, Xu Z Q, Brulet P, Hökfelt T

机构信息

Department of Neuroscience, Karolinska Institute, Stockholm, Sweden.

出版信息

Exp Brain Res. 1996 Nov;112(1):79-88. doi: 10.1007/BF00227180.

DOI:10.1007/BF00227180
PMID:8951409
Abstract

The effect of unilateral transection of the sciatic nerve on expression of immunoreactive galanin (GAL), galanin-message-associated peptide (GMAP) and neuropeptide tyrosine (NPY) in dorsal root ganglia (DRGs) was studied in wild-type mice and in leukemia inhibitory factor (LIF)-deficient mice. In normal and contralateral DRGs small numbers of weakly fluorescent GAL- and GMAP-positive neuronal cell bodies and numerous positive fibers were observed. No NPY-positive cell bodies but a few fibers surrounding blood vessels were seen. In LIF deficient mice hardly any GAL- or GMAP-positive neurons or fibers were seen, nor was NPY-like immunoreactivity present in cell bodies. After axotomy there was a dramatic upregulation of all three peptides in wild-type DRG neurons, whereby 50-60% of the neuron profiles, encompassing both small and large profiles, were GAL- and GMAP-immunoreactive (IR). About one third of all neuron profiles, mainly large ones, were NPY-positive. In LIF-deficient mice this upregulation was much less pronounced. Thus GAL- and GMAP-IR neuron profiles were reduced by 65-70% compared with the wild-type mice. The number of NPY-positive neuron profiles was reduced to half but this difference was not significant. There was also an ipsilateral decrease in fluorescence intensity for all three peptide immunoreactivities in the LIF-deficient mice as compared with wild-type mice after axotomy. There was no apparent difference in size between, respectively, GAL- and GMAP-positive profiles when comparing LIF-deficient and wild-type mice before or after axotomy. There were, however, no small NPY-IR profiles in the LIF-deficient group. The present results suggests that LIF is important for the dramatic upregulation of GAL and GMAP seen after axotomy. It may also be important for the normal expression of galanin in mouse DRGs, since wild-type mice seemed to have somewhat more positive cell bodies and more fluorescent fibers. LIF seems to be less important for the control of NPY synthesis, but may be involved in NPY regulation in small-sized neurons.

摘要

在野生型小鼠和白血病抑制因子(LIF)缺陷型小鼠中,研究了坐骨神经单侧横断对背根神经节(DRG)中免疫反应性甘丙肽(GAL)、甘丙肽信息相关肽(GMAP)和神经肽Y(NPY)表达的影响。在正常和对侧DRG中,观察到少量弱荧光的GAL和GMAP阳性神经元细胞体以及大量阳性纤维。未见NPY阳性细胞体,但可见少数围绕血管的纤维。在LIF缺陷型小鼠中,几乎未见任何GAL或GMAP阳性神经元或纤维,细胞体中也不存在NPY样免疫反应性。轴突切断后,野生型DRG神经元中所有三种肽均显著上调,其中50%-60%的神经元轮廓(包括小轮廓和大轮廓)呈GAL和GMAP免疫反应性(IR)。所有神经元轮廓中约三分之一,主要是大轮廓,呈NPY阳性。在LIF缺陷型小鼠中,这种上调不太明显。因此,与野生型小鼠相比,GAL和GMAP-IR神经元轮廓减少了65%-70%。NPY阳性神经元轮廓的数量减少到一半,但这种差异不显著。与轴突切断后的野生型小鼠相比,LIF缺陷型小鼠中所有三种肽免疫反应性的荧光强度在同侧也有所降低。在轴突切断前后比较LIF缺陷型和野生型小鼠时,GAL和GMAP阳性轮廓的大小没有明显差异。然而,LIF缺陷组中没有小的NPY-IR轮廓。目前的结果表明,LIF对轴突切断后GAL和GMAP的显著上调很重要。它可能对小鼠DRG中甘丙肽的正常表达也很重要,因为野生型小鼠似乎有更多的阳性细胞体和更荧光的纤维。LIF似乎对NPY合成的控制不太重要,但可能参与小尺寸神经元中NPY的调节。

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