Han Ying, Qin Jiong, Chang Xingzhi, Yang Zhixian
Department of Pediatrics, Peking University First Hospital, Beijing 100034, China.
Beijing Da Xue Xue Bao Yi Xue Ban. 2003 Jun 18;35(3):288-91.
To study gamma-aminobutyric acid (GABA) B receptor subunits GABABR1 and GABABR2 protein expression changes after recurrent febrile seizures in the hippocampus of developing rats.
The rats were randomly divided into hyperthermia-treated group (n = 68) and control group (n = 24). According to the times of treatment, and to whether seizures developed, hyperthermia-treated group were subdivided into 4 groups: F1 (febrile, one-time, n = 12), FS1 (febrile seizure, one-time, n = 16), F10 (febrile, ten-time, n = 13), FS10 (febrile seizure, ten-time, n = 15). Immunohistochemical staining was used to demonstrate GABABR1 and GABABR2 expressions in brain sections (12 microns each).
GABABR1 and GABABR2 protein expressions significantly decreased in dentate gyrus and CA1-CA3 neurons in FS10 compared with those in F10, F1, FS1 and control groups. The expressions of GABABR1 and GABABR2 protein showed less intense in F10 than those in FS1, F1 and control groups. No significant differences were observed among F1, FS1 and control group. Throughout the hippocampus, the expressions of GABABR1 and GABABR2 protein largely overlaped. GABABR1 protein expressions decreased seriously as compared with the expressions of GABABR2 protein in dentate gyrus, whereas GABABR2 protein expressions decreased more apparently in hippocampus CA1 and CA3 than that of GABABR1 in FS10.
Recurrent febrile seizures and recurrent hyperthermia all can make the GABABR receptor protein expression down-regulated in the immature rat brain, and GABABR protein expression decreased more apparently in recurrent febrile seizure groups than that in recurrent hyperthermia groups. These suggest that GABABR subunits may play an important role in the immature rat febrile seizures and the difference between GABABR1 and GABABR2 protein expression changes is possible as a result of subunit reorganization, which may lead to the changes of the inhibitory function.
研究发育中大鼠反复热性惊厥后海马中γ-氨基丁酸（GABA）B受体亚基GABABR1和GABABR2蛋白表达的变化。
将大鼠随机分为高温处理组（n = 68）和对照组（n = 24）。根据处理次数以及是否发生惊厥，高温处理组再细分为4组：F1（发热，单次，n = 12）、FS1（热性惊厥，单次，n = 16）、F10（发热，十次，n = 13）、FS10（热性惊厥，十次，n = 15）。采用免疫组织化学染色法检测脑切片（每片12微米）中GABABR1和GABABR2的表达。
与F10、F1、FS1及对照组相比，FS10组齿状回及CA1 - CA3神经元中GABABR1和GABABR2蛋白表达显著降低。F10组中GABABR1和GABABR2蛋白表达强度低于FS1、F1及对照组。F1、FS1及对照组之间未观察到显著差异。在整个海马中，GABABR1和GABABR2蛋白表达大部分重叠。在齿状回中，与GABABR2蛋白表达相比，GABABR1蛋白表达严重降低，而在FS10组海马CA1和CA3中，GABABR2蛋白表达比GABABR1更明显降低。
反复热性惊厥和反复高温均可使未成熟大鼠脑内GABABR受体蛋白表达下调，且反复热性惊厥组GABABR蛋白表达下降比反复高温组更明显。这表明GABABR亚基可能在未成熟大鼠热性惊厥中起重要作用，GABABR1和GABABR2蛋白表达变化的差异可能是亚基重组的结果，这可能导致抑制功能的改变。
