2-Amino-7-phosphonoheptanoic acid, a selective N-methyl-D-aspartate antagonist, blocks swim-induced elevation of cerebellar cyclic guanosine monophosphate.

2-Amino-7-phosphonoheptanoic acid, a selective N-methyl-D-aspartate antagonist, blocks swim-induced elevation of cerebellar cyclic guanosine monophosphate.
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2-氨基-7-膦酰庚酸是一种选择性 N-甲基-D-天冬氨酸拮抗剂,可阻止游泳引起的小脑环单磷酸鸟苷升高。

DOI:
10.1016/0006-8993(86)91251-5
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发表时间:
1986
期刊:
影响因子:
2.9
通讯作者:
Morgan,WW
Morgan,WW
中科院分区:
医学3区
文献类型:
--
作者:
McCaslin,PP;Morgan,WW

文献摘要

相似文献

为了探讨运动活动如何迅速引起小脑环鸟苷一磷酸(CGMP)含量的升高,SD大鼠被要求游泳2.5m~3,游泳1~5圈,代表7~40 S的剧烈活动量。完成游泳任务后,立即用微波照射处死动物,取小脑测定cGMP含量。S游泳一圈的大鼠与不游泳的对照组大鼠小脑cGMP含量无明显差异。然而,在游泳3次和5次的大鼠中,cGMP分别从对照组的1.8倍线性增加到2.4倍。小脑cGMP首次显着升高是在24岁的S(3圈)。在大鼠游泳4圈前,侧脑室注射小剂量NMDA拮抗剂2-氨基-7-膦庚酸(APH),以确定此升高是否与酸性氨基酸途径有关。这一低剂量的APH单独对小脑cGMP含量没有影响,但完全阻断了游泳诱导的该参数的升高。这些数据提供了第一个关于运动活动如何迅速提高小脑cGMP含量的报告,并进一步表明NMDA受体介导的途径参与了活动诱导的该参数的升高。
In order to explore how rapidly locomotor activity induces an elevation in cerebellar cyclic guanosine monophosphate (cGMP) content, Sprague-Dawley rats, pretrained to swim a 2.5-m 3ourse, were required to swim from one to 5 laps representing from 7 to 40 s of strenous activity. Immediately after completing the swimming task, each animal was killed by microwave irradiation and the cerebellum was collected for subsequent determination of the cGMP content. There was no difference in the cerebellar cGMP content between rats swimming one lap, i.e. for 7 s, and control rats that did not swim. However, there was a linear increase in the cGMP over control values from 1.8- to 2.4-fold in rats swimming 3 and 5 times, respectively. The first significant elevation of the cerebellar cGMP was seen at 24 s (3 laps). To determine if acidic amino acid pathways were involved in this elevation, a low dosage of a selective NMDA antagonist, 2-amino-7-phosphonoheptanoic acid (APH) was injected intracerebroventricularly 4 min before having rats swim 4 laps. This low dosage of APH, which alone had no effect on the cerebellar cGMP content, completely blocked the swim-induced elevation of this parameter. These data provide the first report of how quickly locomotor activity elevates the cerebellar cGMP content and further suggest that an NMDA receptor-mediated pathway is involved in the activity-induced elevation of this parameter.