Department of Neurosurgery, Graduate School, Tokyo Medical and Dental University, Tokyo, Japan.
J Clin Neurosci. 2010 May;17(5):612-6. doi: 10.1016/j.jocn.2009.08.011. Epub 2010 Mar 4.
To gain a better understanding of the relationship between epileptogenicity and inhibitory neuronal mechanisms, we examined variations in A1 adenosine (A1A) receptor binding in the hippocampi of rats with spontaneous limbic seizures in the chronic phase after systemic kainic acid treatment. Six weeks after kainate treatment, rats with spontaneous limbic seizures were killed for histological and in vitro autoradiographic analyses of the brain. The analyses were performed using [(3)H] 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), an A1A receptor antagonist. Relative to controls, DPCPX binding was increased in the CA3 region and in the molecular layer of the dentate gyrus in the kainate-treated rats. This is the first evidence of upregulation of the A1A receptor in a model of chronic temporal lobe epilepsy. Increased binding of the A1A receptor may contribute to epileptogenesis in the epileptic focus.
为了更好地理解致痫性与抑制性神经元机制之间的关系，我们研究了在系统给予红藻氨酸后慢性期出现自发性边缘性癫痫发作的大鼠海马中 A1 腺苷（A1A）受体结合的变化。红藻氨酸处理后 6 周，处死出现自发性边缘性癫痫发作的大鼠，对其脑进行组织学和体外放射自显影分析。分析使用 [(3)H]8-环戊基-1,3-二丙基黄嘌呤（DPCPX），即 A1A 受体拮抗剂进行。与对照组相比，DPCPX 结合在红藻氨酸处理大鼠的 CA3 区和齿状回的分子层中增加。这是在慢性颞叶癫痫模型中首次证明 A1A 受体上调。A1A 受体结合的增加可能有助于癫痫灶的癫痫发生。
