Platt K, Butler L S, Bonhaus D W, McNamara J O
J Pharmacol Exp Ther. 1987 Jun;241(3):751-4.
The effects of systemically administered catecholamine receptor antagonists on the anticonvulsant action produced by local application of a gamma-aminobutyric acid agonist, muscimol, to the substantia nigra of rats were studied. Both electroshock and kindled seizures were studied. Two alpha-2 receptor antagonists, idazoxan and yohimbine, blocked the anticonvulsant action of intranigral muscimol in the electroshock model. Neither a beta nor an alpha-1 adrenergic nor a dopamine-2 receptor antagonist blocked this action. In contrast to electroshock seizures, an alpha-2 antagonist only partially reversed the anticonvulsant action of intranigral muscimol in the kindling model. We interpret the data to indicate that the interaction of norepinephrine with alpha-2 receptors is required for the anticonvulsant action of intranigral muscimol in the electroshock model. The only partial reversal found in the kindling model suggests that nigral control of seizure propagation involves more than alpha-2 receptor mediated neurotransmission.
研究了全身给予儿茶酚胺受体拮抗剂对局部应用γ-氨基丁酸激动剂蝇蕈醇至大鼠黑质所产生的抗惊厥作用的影响。对电休克惊厥和点燃性惊厥均进行了研究。两种α-2受体拮抗剂，咪唑克生和育亨宾，在电休克模型中阻断了黑质内蝇蕈醇的抗惊厥作用。β受体拮抗剂、α-1肾上腺素能受体拮抗剂或多巴胺-2受体拮抗剂均未阻断此作用。与电休克惊厥相反，在点燃模型中，α-2拮抗剂仅部分逆转了黑质内蝇蕈醇的抗惊厥作用。我们对这些数据的解释是，在电休克模型中，去甲肾上腺素与α-2受体的相互作用是黑质内蝇蕈醇抗惊厥作用所必需的。在点燃模型中发现的仅部分逆转表明，黑质对癫痫发作传播的控制涉及的不仅仅是α-2受体介导的神经传递。
