ABSTRACT
Diurnal and nocturnal animals differ with respect to the time of day at which the ovulatory surge in luteinizing hormone occurs. In some species this is regulated by the suprachiasmatic nucleus (SCN), the primary circadian clock, via cells that contain vasoactive intestinal polypeptide (VIP) and vasopressin (AVP). Here, we evaluated the hypothesis that chronotype differences in the timing of the luteinizing hormone surge are associated with rhythms in expression of the genes that encode these neuropeptides. Diurnal grass rats (Arvicanthis niloticus) were housed in a 12/12-h light-dark cycle and killed at one of six times of day (Zeitgeber time 1, 5, 9, 13, 17, 21; ZT 0 = lights-on). In-situ hybridization was used to compare levels of vip, avp and VIP receptor mRNA (vipr2) in the SCN of intact females, ovariectomized females, ovariectomized females given estradiol and intact males. We found a sex difference in vip rhythms with a peak occurring at ZT 13 in males and ZT 5 in intact females. In all groups avp mRNA rhythms peaked during the day, from ZT 5 to ZT 9, and had a trough in the dark at ZT 21. There was a modest rhythm and sex difference in the pattern of vipr2. Most importantly, the patterns of each of these SCN rhythms relative to the light-dark cycle resembled those seen in nocturnal rodents. Chronotype differences in timing of neuroendocrine events associated with ovulation are thus likely to be generated downstream of the SCN.
Subject(s)
Arginine Vasopressin/genetics , Circadian Rhythm/genetics , RNA, Messenger/metabolism , Receptors, Vasoactive Intestinal Peptide, Type II/genetics , Suprachiasmatic Nucleus/metabolism , Animals , Arginine Vasopressin/metabolism , Arvicolinae , Estradiol/pharmacology , Estrogens/pharmacology , Female , Gene Expression Regulation/drug effects , Gene Expression Regulation/physiology , Male , Ovariectomy/methods , Receptors, Vasoactive Intestinal Peptide, Type II/metabolism , Sex Characteristics , Sexual Behavior, Animal/physiologyABSTRACT
Sleep deprivation among adolescents is epidemic. We argue that this sleep deprivation is due in part to pubertal changes in the homeostatic and circadian regulation of sleep. These changes promote a delayed sleep phase that is exacerbated by evening light exposure and incompatible with aspects of modern society, notably early school start times. In this review of human and animal literature, we demonstrate that delayed sleep phase during puberty is likely a common phenomenon in mammals, not specific to human adolescents, and we provide insight into the mechanisms underlying this phenomenon.
