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穿孔通路点燃后大鼠海马中GAP - 43和GFAP免疫反应性增加。

Increase in GAP-43 and GFAP immunoreactivity in the rat hippocampus subsequent to perforant path kindling.

作者信息

Dalby N O, Rondouin G, Lerner-Natoli M

机构信息

Institut de Biologie, CNRS UPR9008, INSERMU249, Montpellier, France.

出版信息

J Neurosci Res. 1995 Aug 1;41(5):613-9. doi: 10.1002/jnr.490410507.

DOI:10.1002/jnr.490410507
PMID:7563241
Abstract

Kindling is an animal model of epilepsy which is accompanied by morphological and biochemical changes in the brain, including sprouting of fibers and increased transmitter release. Here we have examined the immunocytochemical expression of 1) GAP-43, a growth-associated protein, which is a neuron-specific PKC substrate, particularly expressed in development and regeneration and 2) glial fibrillary acidic protein (GFAP), part of the astrocytic cytoskeleton, after perforant path kindling. Subsequent to kindling, GAP-43 immunoreactivity was increased in CA1 stratum lacunosum-moleculare and the inner and outer molecular layer of the fascia dentata. Other hippocampal subregions showed a lower increase. GFAP immunoreactivity was increased in the entire hippocampus, but especially in stratum lacunosum-moleculare of the CA1 and the hilus of fascia dentata. The difference between the number of GFAP-positive profiles in the hippocampus of control rats and in fully kindled rats was found to be non-significant. We interpret these findings as being related to both plastic neuronal changes and possible neuronal degeneration.

摘要

点燃效应是一种癫痫动物模型,其伴随着大脑中的形态学和生物化学变化,包括纤维的发芽和递质释放的增加。在此,我们研究了在穿通通路点燃后,1)生长相关蛋白GAP-43(一种神经元特异性蛋白激酶C底物,在发育和再生过程中特别表达)和2)胶质纤维酸性蛋白(GFAP,星形细胞细胞骨架的一部分)的免疫细胞化学表达。点燃后,CA1层的腔隙-分子层以及齿状回的内、外分子层中GAP-43免疫反应性增加。其他海马亚区的增加幅度较小。整个海马中GFAP免疫反应性增加,但特别是在CA1的腔隙-分子层和齿状回的门区。发现对照大鼠海马和完全点燃大鼠海马中GFAP阳性细胞数量的差异不显著。我们将这些发现解释为与可塑性神经元变化和可能的神经元变性都有关。

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