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首页> 外文期刊>The European Journal of Neuroscience >Differential molecular profiles of astrocytes in degeneration and re-innervation after sensory deafferentation of the adult rat cochlear nucleus
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Differential molecular profiles of astrocytes in degeneration and re-innervation after sensory deafferentation of the adult rat cochlear nucleus

机译：成年大鼠耳蜗核感觉减退后星形胶质细胞在变性和重新神经支配中的差异分子谱

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Ablating the cochlea causes total sensory deafferentation of the cochlear nucleus. Over the first postoperative week, degeneration of the auditory nerve and its synaptic terminals in the cochlear nucleus temporally overlaps with its re-innervation by axon collaterals of medial olivocochlear neurons. At the same time, astrocytes increase in size and density. We investigated the time courses of the expression of ezrin, polysialic acid, matrix metalloprotease-9 and matrix metalloprotease-2 within these astrocytes during the first week following cochlear ablation. All four proteins are known to participate in degeneration, regeneration, or both, following injury of the central nervous system. In a next step, stereotaxic injections of kainic acid were made into the ventral nucleus of the trapezoid body prior to cochlear ablation to destroy the neurons that re-innervate the deafferented cochlear nucleus by axon collaterals developing growth-associated protein 43 immunoreactivity. This experimental design allowed us to distinguish between molecular processes associated with degeneration and those associated with re-innervation. Under these conditions, astrocytic growth and proliferation showed an unchanged deafferentation-induced pattern. Similarly, the distribution and amount of ezrin and matrix metalloprotease-9 in astrocytes after cochlear ablation developed in the same way as under cochlear ablation alone. In sharp contrast, the astrocytic expression of polysialic acid and matrix metalloprotease-2 normally invoked by cochlear ablation collapsed when re-innervation of the cochlear nucleus was inhibited by lesioning medial olivocochlear neurons with kainic acid. In conclusion, re-innervation, including axonal growth and synaptogenesis, seems to prompt astrocytes to recompose their molecular profile, paving the way for tissue reorganisation after nerve degeneration and loss of synaptic contacts. Ablating the cochlea of adult rats causes a total sensory deafferentation of the cochlear nucleus. Degeneration of the auditory nerve and its synaptic terminals temporally overlaps with the formation of new synapses in the cochlear nucleus. We show that the process of establishing new synaptic contacts prompts astrocytes to recompose their molecular profile, indicating that they are an integral component of a lesion-induced re-organisation in the adult brain.
机译：消融耳蜗会导致整个耳蜗核的感觉缺失。在术后的第一个星期，听神经及其耳蜗核突触末端的变性在时间上与内侧小乳突神经元轴突侧支的重新支配重叠。同时，星形胶质细胞的大小和密度增加。我们研究了耳蜗消融后第一周内这些星形胶质细胞内ezrin，聚唾液酸，基质金属蛋白酶9和基质金属蛋白酶-2表达的时程。已知所有四种蛋白质在中枢神经系统受伤后均参与变性，再生或两者。在下一步中，在耳蜗消融之前，将立体定向的海藻酸注射剂注入梯形体的腹侧核中，以破坏神经元，该神经元通过轴突侧支重新发育脱去神经力的耳蜗核，从而发展与生长相关的蛋白43的免疫反应性。该实验设计使我们能够区分与变性相关的分子过程与与重新神经相关的分子过程。在这些条件下，星形胶质细胞的生长和增殖表现出不变的脱除咖啡因引起的模式。类似地，耳蜗消融后星形胶质细胞中ezrin和基质金属蛋白酶9的分布和数量与单独进行耳蜗消融的方式相同。与之形成鲜明对比的是，当海藻酸对内侧小核神经元进行损伤抑制时，通常由耳蜗消融激活的聚唾液酸和基质金属蛋白酶2的星形细胞表达瓦解。总之，包括神经轴突生长和突触形成在内的神经支配似乎促使星形胶质细胞重新组成其分子轮廓，为神经变性和突触失去联系后的组织重组铺平了道路。消融成年大鼠的耳蜗会导致整个耳蜗核的感觉缺失。听神经及其突触末端的变性在时间上与耳蜗核中新突触的形成重叠。我们表明建立新的突触接触的过程提示星形胶质细胞重新组成其分子轮廓，表明它们是在成年大脑中病变诱导的重组的不可或缺的组成部分。

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