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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >The novel sigma ligand JO 1994 protects against ischaemia-induced behavioural changes, cell death and receptor dysfunction in the gerbil.
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The novel sigma ligand JO 1994 protects against ischaemia-induced behavioural changes, cell death and receptor dysfunction in the gerbil.

机译：新型sigma配体JO 1994可以防止沙土鼠缺血引起的行为变化，细胞死亡和受体功能障碍。

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摘要

To assess the effects of the novel sigma ligand JO 1994 on behavioural, histological and autoradiographical changes following global ischaemia, the Mongolian gerbil was used. Three experiments were carried out and in each case ischaemia was induced by bilateral carotid occlusion (BCO) for 5 min. In the first experiment we examined the effects of JO 1994 administered at doses of 0.25, 0.5 and 1 mg/kg i.p. 1 h before 5 min BCO on histological parameters 96 h after surgery. In the second experiment the effects of JO 1994 administered at doses of 2.5, 5, 10 and 20 mg/kg i.p. 1 h before 5 min BCO on locomotor activity 24, 48 and 72 h after surgery and on histological parameters 96 h after surgery was examined. In the third experiment the effects of JO 1994 (2.5 and 5 mg/kg i.p.), BMY 14802 (1 and 10 mg/kg i.p.) and MK-801 (2.5 mg/kg i.p.) administered 30 min, 6, 24, 48, 72, 96 and 120 h post-surgery on the densities of M1 and M2 muscarinic receptors in 35 brain regions, 7 days after surgery was examined. Results indicated that 5 min bilateral carotid occluded animals were hyperactive 24, 48 and 72 h after surgery. JO 1994 attenuated this hyperactivity. Extensive neuronal death was observed in the CA1 layer of the hippocampus in 5 min BCO animals 96 h after surgery. The low doses of JO 1994 (0.25, 0.5 and 1 mg/kg) had no effect on the ischaemia-induced cell death. However JO 1994 (2.5, 5, 10 and 20 mg/kg i.p.) protected against the neuronal death of cells in the CA1 layer (P < 0.01-0.03). There was a large loss of M1 and M2 receptors in the CA1 regions of the hippocampus. MK-801, BMY 14802 and JO 1994 provided significant (P < 0.01) protection against this ischaemia-induced receptor loss.
机译：为了评估新型sigma配体JO 1994对全球缺血后行为，组织学和放射自显影变化的影响，使用了蒙古沙鼠。进行了三个实验，每种情况下都是通过双侧颈动脉闭塞（BCO）5分钟诱发局部缺血。在第一个实验中，我们研究了以0.25、0.5和1 mg / kg i.p的剂量施用JO 1994的效果。 BCO 5 min前1 h，术后96 h进行组织学检查。在第二个实验中，JO 1994以2.5、5、10和20 mg / kg i.p.的剂量给药。 BCO 5分钟前1小时检查手术后24、48和72小时的运动能力以及手术后96小时的组织学参数。在第三个实验中，分别在30、6、24、48分钟内分别施用JO 1994（2.5和5 mg / kg ip），BMY 14802（1和10 mg / kg ip）和MK-801（2.5 mg / kg ip）的作用分别于术后7天，术后72、96和120 h对35个脑区M1和M2毒蕈碱受体的密度进行了检查。结果表明，在术后24、48和72 h，双侧颈动脉闭塞动物5 min活跃。 JO 1994减弱了这种多动。术后96小时，在5分钟的BCO动物中，海马CA1层观察到广泛的神经元死亡。 JO 1994的低剂量（0.25、0.5和1 mg / kg）对缺血诱导的细胞死亡没有影响。但是JO 1994（2.5、5、10和20 mg / kg i.p.）可以防止CA1层细胞的神经元死亡（P <0.01-0.03）。海马CA1区的M1和M2受体大量丢失。 MK-801，BMY 14802和JO 1994提供了针对这种缺血引起的受体丢失的显着（P <0.01）保护。

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