Cormier Holly C, Della-Maggiore Valeria, Karatsoreos Ilia N, Koletar Margaret M, Ralph Martin R
Department of Psychology, University of Toronto, 100 St George Street, Toronto, ON, M5S 3G3, Canada.
Eur J Neurosci. 2015 Jan;41(1):79-88. doi: 10.1111/ejn.12637. Epub 2014 Jun 4.
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.
在金黄地鼠(Mesocricetus auratus)中研究了精氨酸加压素在自主运动行为(轮转活动)昼夜节律调节中的作用。全身注射加压素可剂量依赖性地抑制自发夜间跑步,直接向下丘脑视交叉上核微量注射也呈浓度依赖性抑制。预先向视交叉上核注射加压素V1受体拮抗剂可减轻加压素对行为的抑制作用。行为图谱分析显示,外周注射药物主要增加梳理、胁腹标记和睡眠相关行为。中枢注射不会诱导睡眠,但会增加梳理和“安静警觉”(清醒但不动)的时长。外周或中枢注射后的夜间行为模式与未处理动物在夜间轮转跑步开始前一小时的行为模式相似。向内侧视前区或导水管周围灰质进行对照部位的加压素注射会增加胁腹标记和梳理行为,但对运动没有显著影响,这表明视交叉上核附近的加压素靶点具有行为特异性。外周和中枢给药均增加了视交叉上核视网膜接受核心区域中FOS样免疫反应性。FOS阳性细胞的分布与钙结合蛋白亚区域重叠,但范围更广,且大多数钙结合蛋白阳性细胞不共表达FOS。我们提出了一种时间行为调节模型,其中自主行为,如夜间运动活动,受到视交叉上核腹外侧核心区域神经元活动的抑制,这些神经元投射到下丘脑后部,并由来自背内侧壳的节律性加压素输入驱动。