Snead O C, Hechler V, Vergnes M, Marescaux C, Maitre M
Centre de Neurochimie du CNRS, Strasbourg, France.
Epilepsy Res. 1990 Nov;7(2):121-8. doi: 10.1016/0920-1211(90)90097-f.
The distribution and kinetics of specific binding sites for gamma-hydroxybutyrate (GHB), a naturally occurring compound known to produce absence-like seizures, was studied in the brains of Wistar rats with spontaneous, bilaterally synchronous spike wave discharges (SWDs), a model of petit mal epilepsy, and non-epileptic controls using [3H]GHB autoradiography. [3H]GHB receptor binding was increased 40-60% in lateral thalamic nuclei of the epileptic animals. Kinetic analysis showed that the increase in the binding was due to an increase in density of low affinity GHB binding sites in the epileptic animals. Given the ability of GHB to produce petit mal-like seizures when administered to animals, and the fact that the SWDs in the Wistar rat model seem to emanate from lateral thalamus, these data raise the possibility that GHB-mediated mechanisms may play a role in the pathogenesis of petit mal seizures.
γ-羟基丁酸（GHB）是一种天然存在的化合物，已知可引发失神样发作。利用[3H]GHB放射自显影技术，在患有自发性双侧同步棘波放电（SWDs）的Wistar大鼠（一种失神癫痫模型）和非癫痫对照大鼠的大脑中，研究了GHB特异性结合位点的分布和动力学。癫痫动物丘脑外侧核中的[3H]GHB受体结合增加了40%-60%。动力学分析表明，结合增加是由于癫痫动物中低亲和力GHB结合位点的密度增加所致。鉴于给动物注射GHB时它能引发失神样发作，以及Wistar大鼠模型中的SWDs似乎起源于丘脑外侧，这些数据增加了GHB介导的机制可能在失神发作发病机制中起作用的可能性。
