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題名 | The Time Course of Electrophysiological Changes in Rats with Urea-Induced Stimulus Myoclous=尿素誘發刺激性過敏性肌陣攣老鼠的電氣生理學變化之時間經過 |
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作者 | 謝慶良; 唐娜櫻; 林昭庚; 謝慶寶; 飛松省三; 加藤元博; | 書刊名 | 中國醫藥學院雜誌 |
卷期 | 7:3 1998.09[民87.09] |
頁次 | 頁121-126 |
分類號 | 415.9413 |
關鍵詞 | 腦波; 體性感覺誘發電位; 尿素; 肌陣攣; Electroencepha lography; Somatosensory evoked potentials; Urea; Myoclonus; |
語文 | 英文(English) |
中文摘要 | 肌陣攣之病理生理機轉至今仍然不清。本研究是藉著調查尿素誘發刺激性過敏性肌陣攣老鼠的電氣生理學變化之時間經過來了解肌陣攣之發生機轉。我們將12隻Sprague-Dawley的大白鼠分成兩群如下:1)6隻大白鼠用來作為行為觀察,並同時記錄它們的腦波和肌電圖;2)另外6隻大白鼠在清醒狀態下記錄它們的體性感覺誘發電位。我們在完成基準腦波和體性感覺誘發電位記錄之後使用尿素(4.5g/kg)在它們的腹腔注射。我們的結果顯示在尿素注射21±6分後,它們的腦波從每秒鐘6-8Hz 的節律性活動轉變成為每秒鐘2-3Hz 的節律性活動。所有的大白鼠在尿素注射後的30±8分鐘全部發生刺激性過敏性的肌陣攣,其中一隻最後發展成為癲癇發作。基準體性感覺誘發電位是由四個清楚的波型所構成:P1,N1,P2和N2,它們的潛伏期分別為6.5±0.3毫秒,8.3±0.3毫秒,11.0±2.3毫秒和14.4±3.4毫秒。在尿素注射後P1的振幅保留原狀不變,而P1-N1的振幅則緩慢的增加一直到注射後的3小時。N1-P2和P2-N2成份兩者的振幅於尿素注射後呈現快速的增加,於15分鐘時它們的振幅達到最高點,然後下降和消失。 體性感覺誘發電位P1-N1,N1-P2和P2-N2成份的振幅的增大啟示著尿素改變視丘投射系統的活動和大腦皮質的興奮性。基準腦波從每秒6-8Hz的節律性活動變化為每秒2-3Hz和肌陣攣的發生是由於腦幹延髓網狀體神經元的放電。體性感覺誘發電位N1-P2和P2-N2成份的增大在尿素注射後的15分鐘,而腦波轉變成為每秒2-3Hz是21分鐘,隨後在30分鐘時發展為肌陣攣。根據這些發現猜想尿素首先干擾大腦皮質神經元的活動,然後這些干擾影響腦幹網狀體的神經元而導致肌陣攣的發生。 |
英文摘要 | The pathophysiologic mechanisms responsible for myoclonus remain unclear. This study investigated the time course of electrophysiological changes in rats with urea-induced stimulus-myoclonus in order to elucidate the mechanisms involved in myoclonus. A total of 12 Sprague-Dawley (SD) rats were divided into two groups as follows: 1) 6 rats were used for behavioral observation, using electroencephalography (EEG) and electromyography (EMG) recordings simultaneously; 2) Somatosensory evoked potentials (SEPs) recordings were performed in 6 rats without anesthesia. The urea (4.5g/kg) was administered via intraperitoneal injection (i.p.) after baseline EEG and SEPs recordings. The baseline EEG showed that 6-8 Hz rhythmic activity were replaced by 2-3Hz slow rhythmic activity 21±6min after the administration of urea. Then, all of the rats developed stimulus-sensitive myoclonus 30±8min after the administration of urea, and 1 of the 6 rats eventually developed seizure. The baseline SEPs consisted of four distinct components: P1 with a latency of 6.5±0.3 msec( Mean ± SD), N1 with a latency of 8.3±0.3 msec, P2 with a latency of 11.0±2.3 msec and N2 with a latency of 14.4±3.4 msec. The amplitude of P1 remained unchanged, while the amplitude of P1-N1 increased gradually over a 3 hours period after urea administration. Both amplitudes of N1-P2 and P2-N2 components increased rapidly and reached their maximal amplitude 15 min after the administration of urea. These amplitudes then decreased and disappeared. The augmentation of P1-N1, N1-P2 and P2-N2 components of SEPs indicate that urea may alter the activity in the thalamic projection system and the cortical excitability. The baseline EEG of 6-8 Hz rhythmic activity changed to 2-3 Hz and the onset of myoclonus may have resulted from the discharge of brain stem medullary reticular formation. The augmentation of N1-P2 and P2-N2 components of SEPs reached a maximum at 15 min, while EEG changed into slow rhythmic activtiy of 2-3 Hz at 21 min followed by the development of myoclonus at 30 min after urea administration in rats. These findings suggest that urea administration may interfere with activity of neurons in the cerebral cortex first. This interfernce then affects the neurons of the brain stem reticular formation resulting in the development of myoclonus. |
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