中国临床药理学与治疗学
中國臨床藥理學與治療學
중국림상약이학여치료학
CHINESE JOURNAL OF CLINICAL PHARMACOLOGY
2006年
11期
1296-1300
,共5页
前列腺素D2%前列腺素DP受体%睡眠-觉醒%非快动眼睡眠%快动眼睡眠%小鼠
前列腺素D2%前列腺素DP受體%睡眠-覺醒%非快動眼睡眠%快動眼睡眠%小鼠
전렬선소D2%전렬선소DP수체%수면-각성%비쾌동안수면%쾌동안수면%소서
prostaglandin D2%DP receptor%sleep-wake cycle%rapid eye movement sleep%non-rapid eye movement sleep%mice
目的:探讨前列腺素DP受体(DPR)对小鼠睡眠-觉醒调节的影响.方法:在苯巴比妥麻醉下,于DPR基因敲除(KO)小鼠及其野生型(WT)小鼠大脑皮层及颈部肌肉分别植入脑电(Electroencephalogram, EEG)和肌电(Electromyogram, EMG)电极,用EEG/EMG睡眠记录系统于2000时开始连续记录24小时两种小鼠的脑电和肌电波,并用SLEEPSIGN软件进行分析.结果:两种小鼠表现出相同的睡眠-觉醒节律,且明时(800-2000)及暗时(2000-800)时相内两种小鼠的非快动眼(NREM) 睡眠和快动眼(REM)睡眠总量无差异.但与WT 小鼠相比,DPR-KO小鼠明时内的觉醒频率显著增高,NREM睡眠的平均时程显著缩短;且DPR-KO小鼠睡眠呈现低活性的θ波和高活性的δ波.结论:DPR在介导前列腺素D2诱导的睡眠中起着关键性调节作用,缺乏DPR将导致小鼠呈现低强度片段化的NREM睡眠和高警戒状态的REM睡眠.
目的:探討前列腺素DP受體(DPR)對小鼠睡眠-覺醒調節的影響.方法:在苯巴比妥痳醉下,于DPR基因敲除(KO)小鼠及其野生型(WT)小鼠大腦皮層及頸部肌肉分彆植入腦電(Electroencephalogram, EEG)和肌電(Electromyogram, EMG)電極,用EEG/EMG睡眠記錄繫統于2000時開始連續記錄24小時兩種小鼠的腦電和肌電波,併用SLEEPSIGN軟件進行分析.結果:兩種小鼠錶現齣相同的睡眠-覺醒節律,且明時(800-2000)及暗時(2000-800)時相內兩種小鼠的非快動眼(NREM) 睡眠和快動眼(REM)睡眠總量無差異.但與WT 小鼠相比,DPR-KO小鼠明時內的覺醒頻率顯著增高,NREM睡眠的平均時程顯著縮短;且DPR-KO小鼠睡眠呈現低活性的θ波和高活性的δ波.結論:DPR在介導前列腺素D2誘導的睡眠中起著關鍵性調節作用,缺乏DPR將導緻小鼠呈現低彊度片段化的NREM睡眠和高警戒狀態的REM睡眠.
목적:탐토전렬선소DP수체(DPR)대소서수면-각성조절적영향.방법:재분파비타마취하,우DPR기인고제(KO)소서급기야생형(WT)소서대뇌피층급경부기육분별식입뇌전(Electroencephalogram, EEG)화기전(Electromyogram, EMG)전겁,용EEG/EMG수면기록계통우2000시개시련속기록24소시량충소서적뇌전화기전파,병용SLEEPSIGN연건진행분석.결과:량충소서표현출상동적수면-각성절률,차명시(800-2000)급암시(2000-800)시상내량충소서적비쾌동안(NREM) 수면화쾌동안(REM)수면총량무차이.단여WT 소서상비,DPR-KO소서명시내적각성빈솔현저증고,NREM수면적평균시정현저축단;차DPR-KO소서수면정현저활성적θ파화고활성적δ파.결론:DPR재개도전렬선소D2유도적수면중기착관건성조절작용,결핍DPR장도치소서정현저강도편단화적NREM수면화고경계상태적REM수면.
AIM: To investigate the effect of prostanoid DP receptors (DPR) on sleep-wake regulation in mice. METHODS: Under pentobarbital anesthesia, mice were chronically implanted with electroencephalogram (EEG) and electromyogram (EMG) electrodes for polysomnographic recordings. The spontaneous sleep-wake cycles were monitored continuously by EEG/EMG recording system for 24 h beginning at 800 p.m. and analyzed by SLEEPSIGN software in DPR knock out (KO) and wild type (WT) mice. RESULTS: DPR-KO mice exhibited a similar circadian rhythm of sleep-wake cycles to WT mice. The amounts of rapid eye movement (REM) sleep or non-REM (NREM) sleep during both the light and dark periods were identical between the DPR-KO and WT mice. Whereas, an increase in the episode number of wakefulness and a shortage in the duration of NREM sleep were found in DPR-KO mice during the light period compared with WT mice. Moreover, DPR-KO mice showed lower activity in delta-wave component in NREM sleep and higher activity in theta-wave component in REM sleep than WT mice. CONCLUSION: DPR plays a crucial role in mediating the prostaglandin D2-induced sleep. Deficiency of DPR results in the low intensity and fragmented diurnal NREM sleep and the high vigilance REM sleep, with the normal circadian rhythm of sleep in mice.
