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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Studies on the anticonvulsant effect of U50488H on maximal electroshock seizure in mice.
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Studies on the anticonvulsant effect of U50488H on maximal electroshock seizure in mice.

机译：U50488H对小鼠最大电击惊厥的抗惊厥作用研究。

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The present study was designed to investigate the effect of U50488H, a prototype non-peptide kappa opioid agonist on convulsive behaviour using a maximal electroshock (MES) seizure test in mice. An attempt was also made to explore the role of possible receptors involved. MES seizures were induced via transauricular electrodes (60 mA, 0.2 s). Seizure severity was evaluated by means of two parameters, i.e., (1). duration of tonic hindlimb extensor phase and (2). mortality due to convulsions. Intraperitoneal (i.p.) administration of U50488H dose dependently (5-20 mg/kg) decreased the hindlimb extensor phase of MES. The anticonvulsant effect of U50488H was attenuated by the general opioid antagonist, naloxone at a high dose, and by MR2266, a selective kappa antagonist, but not by naltrindole, a delta antagonist. Coadministration of gamma-aminobutyric acid (GABA)ergic drugs (diazepam, GABA, muscimol, and baclofen) and the N-methyl-D-aspartate (NMDA) receptor antagonist, dizocilpine (MK801), with U50488H augmented the anticonvulsant effect of the latter drug in mice. On the other hand, flumazenil, a central benzodiazepine (BZD) receptor antagonist, reversed the protective effect of diazepam and similarly, delta-aminovaleric acid (DAVA), a GABA(B) receptor antagonist, blocked the protective effect of baclofen, a GABA(B) agonist on the anti-MES action of U50488H. These BZD-GABAergic antagonists, namely, flumazenil or DAVA, on their own also counteracted the anti-electroshock seizure effect of U50488H given alone. However, mortality was not significantly altered in any of the above animal groups. Taken together, the findings have shown a possible role for multitude of important neurotransmitter systems, i.e., opioid (kappa), NMDA channel, GABA(A)-BZD-chloride channel complex, and GABA(B) receptors in the anticonvulsant action of U50488H.
机译：本研究旨在使用最大电击（MES）癫痫发作试验研究U50488H（原型非肽Kappa类阿片激动剂）对惊厥行为的影响。还尝试探索可能涉及的受体的作用。 MES发作是通过耳廓电极（60 mA，0.2 s）引起的。通过两个参数，即（1）评估癫痫发作的严重程度。补品后肢伸肌期的持续时间和（2）。抽搐导致的死亡率。腹膜内（i.p.）剂量依赖性（5-20​​ mg / kg）施用U50488H可降低MES的后肢伸肌期。 U50488H的抗惊厥作用被高剂量的普通阿片样物质拮抗剂纳洛酮和选择性Kappa拮抗剂MR2266减弱，但不被δ拮抗剂naltrindole减弱。 γ-氨基丁酸（GABA）药物（地西p，GABA，麝香酚和巴氯芬）与N-甲基-D-天冬氨酸（NMDA）受体拮抗剂双佐西平（MK801）共同给药，与U50488H一起增强后者的抗惊厥作用小鼠中的药物。另一方面，氟马西尼，一种中央苯并二氮杂（BZD）受体拮抗剂，逆转了地西epa的保护作用，同样，δ-氨基戊酸（DAVA），一种GABA（B）受体拮抗剂，阻断了巴氯芬（一种GABA）的保护作用。 （B）关于U50488H的抗MES作用的激动剂。这些BZD-GABA拮抗药，即氟马西尼或DAVA本身也抵消了单独给予的U50488H的抗电击癫痫发作的作用。但是，上述任何一组动物的死亡率都没有显着改变。综上所述，这些发现表明了多种重要的神经递质系统（即阿片类药物（κ），NMDA通道，GABA（A）-BZD-氯离子通道复合物和GABA（B）受体）在U50488H的抗惊厥作用中的可能作用。 。

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