Bregman B, Le Saux F, Trottier S, Chauvel P, Maurin Y
J Neural Transm. 1985;63(2):109-18. doi: 10.1007/BF01252611.
Several studies indicate that brain noradrenaline (NA) depletion facilitates the occurrence of epileptogenic syndromes in various animal models. In cobalt-induced epilepsy in the rat activity is associated with a cortical NA denervation. In order to search for cortical adrenoceptor modifications, inonophoretic studies and adrenoceptor binding assays were performed. At the period of maximal seizure activity, there was a significant supersensitivity of cortical neurons to the ionophoretic application of NA. An increase in the density of beta-adrenoceptor binding sites was observed. No modification in alpha 1- and alpha 2-adrenoceptor binding sites was found. This suggests that in cobalt-induced epilepsy there is a denervation supersensitivity which rests on a selective involvement of beta-adrenoceptors.
多项研究表明,脑去甲肾上腺素(NA)耗竭会促进各种动物模型中癫痫综合征的发生。在大鼠钴诱导的癫痫中,活动与皮质NA去神经支配有关。为了寻找皮质肾上腺素能受体的改变,进行了离子电泳研究和肾上腺素能受体结合试验。在癫痫活动最强的时期,皮质神经元对NA的离子电泳应用表现出明显的超敏反应。观察到β-肾上腺素能受体结合位点密度增加。未发现α1和α2肾上腺素能受体结合位点有改变。这表明在钴诱导的癫痫中存在去神经超敏反应,其基于β-肾上腺素能受体的选择性参与。