c—fos基因在听源性惊厥易感大鼠脑的表达：原位杂交组织化学…

运用原位杂交技术，以遗传性源性惊厥易感大鼠Ｐ７７ＰＭＣ为对象，发现听源性惊厥可诱导大鼠脑内ｃ－ｆｏｓ基因快速、大量、短暂性表达。ｃ－ｆｏｓｍＲＮＡ分布于大脑皮层、梨状皮层、杏仁香体、海马齿状回、上丘脑、背侧丘脑、正丘脑部分核团、下丘、蜗神经核蓝斑及小脑等处。惊厥后皮层下结构中ｃ－ｆｏｓ基因表达变化程度超过皮层的变化，尤其是下丘，蜗神经与惊厥时程有明显关系。推测皮层下结构对听源性惊厥的发生有重要意义     

听源性惊厥易感大鼠惊厥和点燃后听觉核团内的c—fos表达

为探讨听源性惊厥点燃和听觉核团的关系，用免疫细胞化学方法结合体视学分析，研究了Ｗｉｓｔａｒ种系的听源性惊厥易感大鼠惊厥和点燃后听觉核团内ｃ－ｆｏｓ表达的差异。在内侧膝状体背侧核和蜗神经背核，Ｆｏｓ标记细胞无显著变化。本研究结果表明，听源性惊厥导的display status     

SOMAN诱发惊厥大鼠丘脑内c－fos的表达

用ＡＢＣ免疫组化技术研究了Ｓｏｍａｎ诱发大鼠产生强直阵挛性惊厥后的ｃ－ｆｏｓ原癌基因在丘脑中的表达。结果显示：在低剂量Ｓｏｍａｎ中毒但未出现惊厥的动物和戊巴比妥抗惊厥的动物丘脑内都未见ｃ－ｆｏｓ表达的增加。而致惊厥的动物则从惊厥１ｈ至３ｈ，丘脑内ｃ－ｆｏｓ表达均有显著增加，表达呈恒定的核特异定位分布。出现群集ＦＯＳ样免疫阳性神经元的核团是：丘脑中线核群的丘脑室旁核、菱形核、粘合核；板内核群的中央旁核、中央内侧核和中央外侧核；丘脑前核诸亚核以及丘脑网状核。上述结果表明，丘脑非特异性核团的协同活动以及丘脑前核可能参与惊厥活动的整合。     

SOMAN诱发惊厥大鼠丘脑内c－fos的表达

用ＡＢＣ免疫组化技术研究了Ｓｏｍａｎ诱发大鼠产生强直阵挛性惊厥后的ｃ－ｆｏｓ原癌基因在丘脑中的表达。结果显示：在低剂量Ｓｏｍａｎ中毒但未出现惊厥的动物和戊巴比妥抗惊厥的动物丘脑内都未见ｃ－ｆｏｓ表达的增加。而致惊厥的动物则从惊厥１ｈ至３ｈ，丘脑内ｃ－ｆｏｓ表达均有显著增加，表达呈恒定的核特异定位分布。出现群集ＦＯＳ样免疫阳性神经元的核团是：丘脑中线核群的丘脑室旁核、菱形核、粘合核；板内核群的中央旁核、中央内侧核和中央外侧核；丘脑前核诸亚核以及丘脑网状核。上述结果表明，丘脑非特异性核团的协同活动以及丘脑前核可能参与惊厥活动的整合。     

听源性惊厥上调惊厥易感大鼠脑内NR1基因的表达

N-甲基-D-门冬氨酸受体（NMDA或NR）功能的变化与癫痫的发生和发展密切相关．本文用原位杂交技术探讨了遗传癫痫易感大鼠P77PMC惊厥后不同时间NRI亚基基因表达状况，证明：大脑皮层，海马齿状回，CA1、CA2、CA3及下丘NR1mRNA表达呈时间依赖性增高，下丘在惊厥后2h即出现NR1mRNA高表，而大脑皮层和海马各区域24h达高峰．听源性惊厥后这些区域NR1mRNA表达的上调可能与神经网络兴奋性增高及癫痫易感性的保持有关。     

听源性惊厥易感大鼠室旁核神经元c—fos表达的研究

目的为下丘脑室旁核参与惊厥应答提供形态学资料。方法：以听源性忭厥易大鼠为动物模型，用免疫组织化学ＡＢＣ法显示下丘脑室旁核神经元即早基因ｃ－ｆｏｓ的表达。     

听源性惊厥发作后中脑导水管周围灰质内c-fos基因的变化

目的 探讨中脑导水管周围灰质（ＰＡＧ）与听源性惊厥的关系。方法 用神经细胞Ｚ（Ｎｉｓｓｌ）染色和免疫细胞化学技术,观察听源性惊厥发作后易感大鼠（Ｐ７７ＰＭＣ）ＰＡＧ内即早基因ｃ－ｆｏｓ的表达情况。结果 听源性惊厥发作２ｈ后,Ｐ７７ＰＭＣ大鼠ＰＡＧ的背侧亚区及背外侧亚区,尾侧段腹外侧亚区内出现大量Ｆｏｓ阳性神经元,Ｆｏｓ阳性神经元百分率显著高于对照组。     

听源性惊厥易感大鼠惊厥和点燃后前脑结构内的c—fos表达

为探讨听源性惊厥点燃和前脑结构的关系，用免疫细胞化学方法结合体视学分析，研究Ｗｉｓｔａｒ种系的听源性惊厥易感大鼠惊厥和点燃后，前脑结构内ｃ－ｆｏｓ表达的差异。结果显示，１．正常Ｗｉｓｔａｒ大鼠接受一次强音刺激后，海马，齿状回，杏仁核，内嗅皮质，嗅周皮质和额－顶皮质内未见Ｆｏｘ阳性神经元；２．Ｐ７７ＰＭＣ大鼠一次惊厥后，除海马，齿状回外，上述被检各区内可见广泛的Ｆｏｓ阳性神经元，其分布具有区域差异．     

压力负荷下大鼠主动脉平滑细胞fos基因表达

压力负荷下大鼠主动脉平滑细胞ｆｏｓ基因表达张放鸣，何光篪，刘正津第三军医大学重庆６３００３８以（３５）Ｓ标记的ｃ－ｆｏｓ为探针用原位杂交的方法研究压力负荷下大鼠主动脉平滑肌的基因表达，在分子水平探讨力对平滑肌细胞增殖的影响。实验结果表明：正常情况下，...     

胶质瘤细胞c—fos和c—myc基因表达与血小板源生长因子B链的？…

目的 探讨胶质瘤细胞ｃ－ｆｏｓ和ｃ－ｍｙｃ基因表达和血小板源生长因子Ｂ链的纯合二聚体自分泌环活性的改变及其相互关系。方法 用原位杂交和免疫组化方法观察了６７例人胶质瘤组织。结果 ６７例中,ｃ－ｆｏｓ ｍＲＮＡ,ｃ－ｆｏｓ蛋白,ｃ－ｍｙｃ ｍＲＮＡ及ｃ－ｍｙｃ蛋白阳性率分别为;１００％,１００％,８５．１％,８３．６％。     

惊厥对神经元缝隙连接蛋白基因表达的影响

神经元之间的缝隙连接蛋白Cx32是形成电突触的结构基础,电突触参与惊厥时神经元的同步化放电过程。为探讨惊厥对脑内神经元Cx32基因表达的影响,以遗传性癫痫易感大鼠P77PMC为模型,采用原位杂交的方法观察P77PMC大鼠听源性惊厥后脑内Cx32基因表达的变化。原位杂交结果显示：惊厥后在大脑皮层,海马脑区Cx32mRNA表达呈时间依赖性上调,惊厥后4h表达量明显增加,24h达高峰,结果提示：惊厥能上调神经元Cx32mRNA表达,从而可能使神经元之间的电突触联系增加,有利于神经元的同步化放电,加重惊厥的发生发展。     

The use of neural transplantation for suppression of seizure activity in genetically epilepsy-prone rats

The possibility of correcting seizure activity with neural transplantation was studied in Wistar rats with audiogenic seizures and in Krushinskii-Molodkina rats with high level of audiogenic seizures. In Wistar rats seizures were absent during 24 weeks after combined bilateral transplantation of striatal and cerebellar tissue from newborn rats into the parietal cortex. The same transplantation performed in Krushinskii--Molodkina rats increased the latency of audiogenic seizures. In some rats the intensity of seizures decreased, but they did not completely disappeared. Suppression of seizure activity in Krushinskii-Molodkina rats was observed after transplantation of striatal and cerebellar tissue simultaneously into the parietal cortex and inferior colliculi.     

P77PMC大鼠听源性惊厥神经回路──核团损毁研究

采用立体定位直流电损毁法,分别损毁双侧下丘、脑桥吻侧网状核、内侧膝状体、黑质,观察核团损毁对大鼠听源性惊厥行为的影响,以寻找与P77PMC大鼠听源性惊厥有关的神经核团。结果表明：双侧下丘损毁后能完全阻断强直阵挛性惊厥,脑桥吻侧网状核损毁能明显减少惊厥发生（P＜0．05）,而双侧内侧膝状体及黑质损毁对惊厥无明显影响（P＜0．05）。提示下丘是P77PMC大鼠听源性惊厥的关键核团,而脑桥吻侧网状核可能参与了惊厥回路,内侧膝状体可能并未参与惊厥回路,黑质在此惊厥中的作用尚不明确。     

The use of neural transplantation for suppression of seizure activity in genetically epilepsy-prone rats

The possibility of correcting seizure activity with neural transplantation was studied in Wistar rats with audiogenic seizures and in Krushinskii-Molodkina rats with high level of audiogenic seizures. In Wistar rats seizures were absent during 24 weeks after combined bilateral transplantation of striatal and cerebellar tissue from newborn rats into the parietal cortex. The same transplantation performed in Krushinskii-Molodkina rats increased the latency of audiogenic seizures. In some rats the intensity of seizures decreased, but they did not completely disappeared. Suppression of seizure activity in Krushinskii-Molodkina rats was observed after transplantation of striatal and cerebellar tissue simultaneously into the parietal cortex and inferior colliculi. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 130, No. 9, pp. 279–283, September, 2000     

Altered tone-induced Fos expression in the mouse inferior colliculus after early exposure to intense noise

Mice become highly susceptible to audiogenic seizures (AGS) after being exposed to intense, high-frequency noise during a critical period of early life (priming). To determine the critical site for AGS priming in the auditory brainstem, animals in the experimental group were primed at 21 days, and the tone-induced Fos immunoreactivity was examined 1, 7, and 14 days after priming as an index of excitability of neurons. Enhanced Fos immunoreactivity was observed in the inferior colliculus (IC) of the primed mice 7 and 14 days after priming as compared to that of non-primed mice and attenuated Fos expression was observed 1 day after priming. No significant elevation of Fos expression was observed in the cochlear nucleus and the deep layer of the superior colliculus of either type of mice. These results strongly suggest that the IC is the target site of AGS priming.