Melatonin and its new agonist S-20098 restore synchronized sleep fragmented by experimental trypanosome infection in the rat
Melatonin and its new agonist S-20098 restore synchronized sleep fragmented by experimental trypanosome infection in the rat
复制标题
DOI：
10.1016/0361-9230(95)02032-2
复制
发表时间：
1996-01-01
影响因子：
3.8
通讯作者：
Bentivoglio, M
中科院分区：
文献类型：
--
作者：
GrassiZucconi, G;Semprevivo, M;Bentivoglio, M
布氏锥虫在大鼠体内的实验性感染为睡眠调节机制的功能障碍提供了一个独特的模型，因为同步睡眠发作的长度在疾病的晚期被选择性地显著减少。在本研究中，在睡眠开始前，对感染锥虫的大鼠急性给予褪黑素（3mg /kg SC）。这种治疗导致受感染的动物和只接受载体的动物同步睡眠时间的显著增加。因此，褪黑素在感染期间恢复了正常的睡眠模式。新的褪黑激素激动剂S-20098也获得了类似的结果。褪黑素或S-20098急性给药对未感染动物的睡眠参数没有显著改变。这些结果表明外源性褪黑激素和S-20098对实验性锥虫病睡眠片段化有选择性调节作用。
The experimental infection with the parasite Trypanosoma brucei in the rat provides a unique model of dysfunction of the sleep regulatory mechanisms, because the length of synchronized sleep episodes is selectively and dramatically reduced in the advanced stages of the disease. In the present study, melatonin was acutely administered (3 mg/kg SC) to trypanosome-infected rats, before the sleep onset. This treatment resulted in a significant increase of the length of synchronized sleep episodes in respect to the infected animals and to those that had received only the vehicle. Thus, melatonin restored a normal sleep pattern during the infection. Similar findings were obtained with the new melatonin agonist S-20098. The sleep parameters were not significantly modified by either melatonin or S-20098 acute administration to noninfected animals. These findings indicate that exogenous melatonin and S-20098 exert a selective regulatory action on sleep fragmentation during experimental trypanosomiasis.