SEIZURES INCREASE BASIC FIBROBLAST GROWTH-FACTOR MESSENGER-RNA IN ADULT-RAT FOREBRAIN NEURONS AND GLIA

SEIZURES INCREASE BASIC FIBROBLAST GROWTH-FACTOR MESSENGER-RNA IN ADULT-RAT FOREBRAIN NEURONS AND GLIA
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DOI:
10.1016/0169-328x(94)90250-x
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发表时间:
1994-02-01
期刊:
MOLECULAR BRAIN RESEARCH
影响因子:
--
通讯作者:
ISACKSON, PJ
ISACKSON, PJ
中科院分区:
其他
文献类型:
--
作者:
GALL, CM;BERSCHAUER, R;ISACKSON, PJ

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采用原位杂交技术和S1核酸酶保护技术,观察碱性成纤维细胞生长因子(bFGF) mRNA在正常大鼠前脑中的分布及反复发作对bFGF mRNA表达的影响。在未治疗的成年大鼠中,s -35标记的bFGF cRNA杂交密集标记了几个离散区域的神经元,包括裂谷、灰工业、海马层锥体区域CA2和rostromedial CA1。枕下前和枕内侧齿状回颗粒层的神经元被轻度标记。此外,放射自显影标记在海马分子层、嗅皮层I层和嗅神经层等区域的弥漫性分布提示定位于胶质细胞。铂丝肝门病变,没有引起癫痫发作,仅在同侧半球原发性和继发性变性区域增加了神经胶质细胞的cRNA杂交;在这些损伤控制的大鼠中,神经元的杂交没有明显增加。局灶性不锈钢丝肝门病变在病变后2-10小时引起反复发作,海马、新皮质、嗅皮质、杏仁核和隔区cRNA杂交双侧分布升高。这些癫痫依赖的杂交增加在病变后6小时明显,在病变后12至24小时达到最大,并在4天后下降到接近对照水平。在大多数区域,杂交升高似乎主要与星形胶质细胞有关,但在病变后12和24小时牺牲的实验性癫痫大鼠中,齿状回颗粒细胞和嗅觉皮质神经元的杂交也明显增加。这些结果表明,复发性癫痫发作增加了前脑神经元和胶质细胞中bFGF mRNA的表达,并暗示bFGF参与了癫痫发作后前脑神经元生物合成活性的其他变化。
The distribution of basic fibroblast growth factor (bFGF) mRNA in normal rat forebrain, and the influence of recurrent seizure activity on the expression of this mRNA, was evaluated using in situ hybridization and S1 nuclease protection techniques. In the untreated adult rat, hybridization of S-35-labeled bFGF cRNA densely labeled neurons in a few discrete areas including the tenia tecta, indusium gresium, and hippocampal stratum pyramidale of regions CA2 and rostromedial CA1. Neurons in the prosubiculum and rostromedial dentate gyrus stratum granulosum were lightly labeled. In addition, a diffuse distribution of autoradiographic labeling in areas such as the hippocampal molecular layers, olfactory cortical layer I, and the olfactory nerve layer was suggestive of localization in glial cells. Platinum wire hilar lesions, which did not induce seizures, increased cRNA hybridization in glial cells in primary and secondary areas of degeneration in the ipsilateral hemisphere only; hybridization was not noticeably increased in neurons in these lesion-control rats. Focal stainless-steel wire hilar lesions, which caused recurrent seizures 2-10 h postlesion, induced bilaterally distributed increases in cRNA hybridization in hippocampus, neocortex, olfactory cortex, amygdala, and septum. These seizure-dependent increases in hybridization were evident 6 h postlesion, were maximal from 12 to 24 h postlesion, and declined to near control levels by 4 days. In most regions the elevated hybridization appeared to be associated primarily with astroglia but in experimental seizure rats sacrificed 12 and 24 h postlesion hybridization was also markedly increased in the dentate gyrus granule cells and olfactory cortical neurons. These results demonstrate that recurrent seizures increase bFGF mRNA expression by both forebrain neurons and glia and implicate bFGF in the coordination of other changes in the biosynthetic activities of forebrain neurons that occur after seizures.