Savage D D, McNamara J O
J Pharmacol Exp Ther. 1982 Sep;222(3):670-3.
Amygdala-kindled seizures reduced significantly the total number of [3H]quinuclidinyl benzilate binding sites in both dentate and hippocampal gyri compared to electrode implanted unstimulated controls. Both high and low affinity carbachol displaceable binding site populations were significantly reduced in hippocampal gyrus. By contrast, a selective decline of low affinity sites was found in dentate gyrus membranes. The selectivity of the decline in dentate but not hippocampus gyrus underscores the specificity of this molecular response to amygdala-kindled seizures. We suggest that these receptor alterations underlie adaptive mechanisms which antagonize kindled epileptogenesis.
与植入电极但未受刺激的对照组相比，杏仁核点燃癫痫发作显著减少了齿状回和海马回中[3H]喹核醇基苯甲酸酯结合位点的总数。海马回中高亲和力和低亲和力的卡巴胆碱可置换结合位点群体均显著减少。相比之下，在齿状回膜中发现低亲和力位点有选择性下降。齿状回而非海马回中结合位点下降的选择性强调了这种分子反应对杏仁核点燃癫痫发作的特异性。我们认为这些受体改变是对抗点燃癫痫发生的适应性机制的基础。
