Baimbridge K G, Mody I, Miller J J
Epilepsia. 1985 Sep-Oct;26(5):460-5. doi: 10.1111/j.1528-1157.1985.tb05681.x.
The calcium-binding protein (CaBP) content of the hippocampal formation was determined by radioimmunoassay in control and kindled rats. Kindling of a number of different sites resulted in a reduction in the CaBP content of the hippocampal formation, which was shown immunohistochemically to be restricted to the dentate granule cells and their processes. The maximum decline in CaBP varied with the different kindling sites: perforant path, 33%; commissural path, 32%; septum, 30%; amygdala, 18%; and olfactory bulbs, 15%. There were no changes in the CaBP content of the stimulated areas themselves. In cases where the kindling stimulus was delivered unilaterally (perforant path and amygdala), the maximum decrease in hippocampal CaBP was observed ipsilateral to the site of stimulation when the criterion for full kindling was established (six consecutive stage 5 motor seizures). Further kindling trials were required to produce a similar magnitude decrease in the CaBP content of the contralateral hippocampus. These observations are discussed both in relation to the possible role of CaBP in the establishment of a seizure response to kindling and also as a potential compensatory mechanism that may serve to overcome the epileptogenic effects of kindling.
通过放射免疫分析法测定了对照大鼠和点燃大鼠海马结构中的钙结合蛋白（CaBP）含量。对多个不同部位进行点燃会导致海马结构中CaBP含量降低，免疫组织化学显示这种降低仅限于齿状颗粒细胞及其突起。CaBP的最大降幅因点燃部位不同而有所差异：穿通通路为33%；连合通路为32%；隔区为30%；杏仁核为18%；嗅球为15%。受刺激区域本身的CaBP含量没有变化。在单侧给予点燃刺激的情况下（穿通通路和杏仁核），当确立完全点燃的标准（连续6次5期运动性癫痫发作）时，在刺激部位同侧观察到海马CaBP的最大降幅。需要进一步的点燃试验才能使对侧海马的CaBP含量产生类似幅度的降低。本文将这些观察结果与CaBP在对点燃产生癫痫发作反应的建立中可能发挥的作用以及作为一种可能用于克服点燃致痫作用的潜在补偿机制进行了讨论。
