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首页> 外文期刊>The European Journal of Neuroscience >Suprachiasmatic vasopressin and the circadian regulation of voluntary locomotor behavior
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Suprachiasmatic vasopressin and the circadian regulation of voluntary locomotor behavior

机译:超视交叉加压素和自发运动行为的昼夜节律

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A role for arginine vasopressin in the circadian regulation of voluntary locomotor behavior (wheel running activity) was investigated in the golden hamster, Mesocricetus auratus. Spontaneous nocturnal running was suppressed in a dose-dependent manner by systemic injections of vasopressin, and also in a concentration-dependent manner by microinjections directly into the hypothalamic suprachiasmatic nucleus. Pre-injections of a vasopressin V1 receptor antagonist into the nucleus reduced the suppression of behavior by vasopressin. Ethogram analyses revealed that peripheral drug injections predominantly increased grooming, flank marking, and sleep-related behaviors. Central injections did not induce sleep, but increased grooming and periods of quiet vigilance' (awake but not moving). Nocturnal behavioral profiles following either peripheral or central injections were similar to those shown by untreated animals in the hour prior to the onset of nocturnal wheel running. Site control vasopressin injections into the medial preoptic area or periaqueductal gray increased flank marking and grooming, but had no significant effect on locomotion, suggesting behavioral specificity of a vasopressin target near the suprachiasmatic nucleus. Both peripheral and central administration increased FOS-like immunoreactivity in the retinorecipient core of the suprachiasmatic nucleus. The distribution of FOS-positive cells overlapped the calbindin subregion, but was more extensive, and most calbindin-positive cells did not co-express FOS. We propose a model of temporal behavioral regulation wherein voluntary behavior, such as nocturnal locomotor activity, is inhibited by the activity of neurons in the suprachiasmatic ventrolateral core that project to the posterior hypothalamus and are driven by rhythmic vasopressin input from the dorsomedial shell.
机译:在金色仓鼠中金龟子中研究了精氨酸加压素在昼夜调节自主运动行为(车轮行驶活动)中的作用。通过全身性加压素的注射以剂量依赖性的方式抑制自发性夜行性,并且通过直接注射到下丘脑上视交叉核中以浓度依赖性的方式来抑制自发性夜行性。向血管核中预注射加压素V1受体拮抗剂可降低加压素对行为的抑制作用。人口统计学分析表明,外围药物注射主要增加了修饰,侧面标志和与睡眠有关的行为。中央注射不会引起睡眠,但会增加梳理和保持安静状态的警觉(清醒但不动)。夜间或轮流注射后的夜间行为特征与夜间轮运行开始前一个小时内未经治疗的动物所显示的相似。在视前内侧区域或导水管周围灰色部位进行加压素加压素注射可增加侧翼标记和修饰,但对运动没有明显影响,提示在视交叉上核附近加压素靶的行为特异性。外周和中央给药都增加了视交叉上核的视网膜受体核心中的FOS样免疫反应性。 FOS阳性细胞的分布与calbindin子区域重叠,但分布更为广泛,大多数calbindin阳性细胞并不共表达FOS。我们提出了一种时间行为调节模型,其中自愿行为(例如夜间运动功能)受到束缚上丘脑腹侧后核的神经元活动的抑制,该神经元投射到下丘脑后部,并由有脉的加压素从背壳输入。

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