Ekonomou A, Angelatou F, Vergnes M, Kostopoulos G
Department of Physiology, School of Medicine, University of Patras, Greece.
Neuroreport. 1998 Jun 22;9(9):2135-40. doi: 10.1097/00001756-199806220-00042.
The possible involvement of the adenosinergic modulatory system in the pathogenesis of absence seizures was investigated in genetic absence epilepsy rats from Strasbourg (GAERS). Using in vitro quantitative autoradiography, the distribution of A1 adenosine receptors and adenosine uptake sites in the brain of GAERS was studied and compared to that of control animals. An area-specific lower density of A1 receptors (15% decrease) was detected in reticular (nRT) and anterior ventral (AV) thalamic nuclei as well as basal ganglia in the brains of GAERS animals compared with control animals. Since adenosine exerts an anti-oscillatory effect on the thalamic nuclei by suppressing (via A1 receptors) excitatory as well as inhibitory neurotransmitter release, the impairment in A1 receptor density seen here, especially in nRT, could be implicated in the thalamic rhythmicity underlying spike and wave discharges present in this absence epilepsy model.
在来自斯特拉斯堡的遗传性失神癫痫大鼠(GAERS)中,研究了腺苷能调节系统在失神发作发病机制中的可能作用。采用体外定量放射自显影技术,研究了GAERS大鼠脑内A1腺苷受体和腺苷摄取位点的分布,并与对照动物进行比较。与对照动物相比,在GAERS动物脑内的网状丘脑核(nRT)、丘脑前腹核(AV)以及基底神经节中检测到A1受体的区域特异性低密度(降低15%)。由于腺苷通过抑制(经由A1受体)兴奋性和抑制性神经递质释放,对丘脑核发挥抗振荡作用,因此此处观察到的A1受体密度受损,尤其是在nRT中,可能与该失神癫痫模型中棘波和慢波放电所基于的丘脑节律性有关。