Gall C M, Berschauer R, Isackson P J
Department of Anatomy and Neurobiology, University of California, Irvine 92717.
Brain Res Mol Brain Res. 1994 Feb;21(3-4):190-205. doi: 10.1016/0169-328x(94)90250-x.
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 35S-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.
运用原位杂交和S1核酸酶保护技术，评估了碱性成纤维细胞生长因子（bFGF）mRNA在正常大鼠前脑的分布，以及反复癫痫发作活动对该mRNA表达的影响。在未经处理的成年大鼠中，35S标记的bFGF cRNA杂交，在包括终板带、灰被、CA2区和CA1区喙内侧海马锥体层等几个离散区域密集标记神经元。前下托和齿状回喙内侧颗粒层的神经元被轻度标记。此外，在海马分子层、嗅皮质I层和嗅神经层等区域放射自显影标记的弥漫分布提示其定位于神经胶质细胞。铂丝海马门区损伤未诱发癫痫发作，仅使同侧半球初级和次级变性区域的神经胶质细胞中cRNA杂交增加；在这些损伤对照大鼠的神经元中，杂交没有明显增加。局灶性不锈钢丝海马门区损伤在损伤后2 - 10小时引起反复癫痫发作，诱导海马、新皮质、嗅皮质、杏仁核和隔区cRNA杂交呈双侧分布增加。这些与癫痫发作相关的杂交增加在损伤后6小时明显，在损伤后12至24小时达到最大，到4天时降至接近对照水平。在大多数区域，杂交升高似乎主要与星形胶质细胞有关，但在损伤后12小时和24小时处死的实验性癫痫大鼠中，齿状回颗粒细胞和嗅皮质神经元中的杂交也明显增加。这些结果表明，反复癫痫发作可增加前脑神经元和神经胶质细胞中bFGF mRNA的表达，并提示bFGF参与癫痫发作后前脑神经元生物合成活动中其他变化的协调。
