失神性癫痫持续发作诱导丘脑C-fos基因表达的实验研究

C-fos oncogene expression in γ-Hydroxybutyrate induced generalized absence epilepsy in thalamus of the rat.

目的 探讨失神性癫痫持续发作的病理生理机制。 方法 采用C -fos基因探针原位杂交法在γ -羟丁酸诱发的大鼠失神性癫痫持续发作模型上 ,观察癫痫持续发作后不同时间丘脑各核团中C -fos基因表达的分布状况 ,用C -fos基因阳性细胞密度作定量研究指标。 结果 失神性癫痫发作后 1 0min ,双侧丘脑室旁核内可见到低密度C -fos阳性细胞 ;3 0min时 ,高密度C -fos阳性细胞广泛分布于外侧缰核、室旁核、菱形核和丘脑板内核群。 结论 外侧缰核及丘脑中线和板内核群极可能涉及失神性癫痫发作的病理生理机制。

Objective To explore the pathophysiological mechanisms of absence seizures. Methods Using the model of gamma hydroxybutyrate (GHB) induced generalized absence epilepsy, the present work investigated the distribution of C fos oncogene expression in the rat thalamus with C fos probe in situ hybridization. Results Ten minutes following absence like seizures, low density C fos positive cells were found in bilateral thalamic paraventricular nuclei (PV).30 minutes After absence seizures, high density C fos positive cells were observed in bilaterally late^ral habenular nucleus (LHb), PV, rhomboid thalamic nuleus, and intralaminar nuclei of the thalamus. Conclusions The LHb, the midline and intralaminar thalamic nuclei may be involved in the pathophysiology process of absence seizures.