Circadian rhythm

About: Circadian rhythm is a research topic. Over the lifetime, 26606 publications have been published within this topic receiving 1104974 citations. The topic is also known as: GO:0007623 & circadian cycle.

Hypothalamic regulation of sleep and circadian rhythms

Abstract: A series of findings over the past decade has begun to identify the brain circuitry and neurotransmitters that regulate our daily cycles of sleep and wakefulness. The latter depends on a network of cell groups that activate the thalamus and the cerebral cortex. A key switch in the hypothalamus shuts off this arousal system during sleep. Other hypothalamic neurons stabilize the switch, and their absence results in inappropriate switching of behavioural states, such as occurs in narcolepsy. These findings explain how various drugs affect sleep and wakefulness, and provide the basis for a wide range of environmental influences to shape wake-sleep cycles into the optimal pattern for survival.

Obesity and Metabolic Syndrome in Circadian Clock Mutant Mice

Abstract: The CLOCK transcription factor is a key component of the molecular circadian clock within pacemaker neurons of the hypothalamic suprachiasmatic nucleus. We found that homozygous Clock mutant mice have a greatly attenuated diurnal feeding rhythm, are hyperphagic and obese, and develop a metabolic syndrome of hyperleptinemia, hyperlipidemia, hepatic steatosis, hyperglycemia, and hypoinsulinemia. Expression of transcripts encoding selected hypothalamic peptides associated with energy balance was attenuated in the Clock mutant mice. These results suggest that the circadian clock gene network plays an important role in mammalian energy balance.

Coordinated transcription of key pathways in the mouse by the circadian clock.

Abstract: In mammals, circadian control of physiology and behavior is driven by a master pacemaker located in the suprachiasmatic nuclei (SCN) of the hypothalamus. We have used gene expression profiling to identify cycling transcripts in the SCN and in the liver. Our analysis revealed approximately 650 cycling transcripts and showed that the majority of these were specific to either the SCN or the liver. Genetic and genomic analysis suggests that a relatively small number of output genes are directly regulated by core oscillator components. Major processes regulated by the SCN and liver were found to be under circadian regulation. Importantly, rate-limiting steps in these various pathways were key sites of circadian control, highlighting the fundamental role that circadian clocks play in cellular and organismal physiology.

Restricted feeding uncouples circadian oscillators in peripheral tissues from the central pacemaker in the suprachiasmatic nucleus

Abstract: In mammals, circadian oscillators exist not only in the suprachiasmatic nucleus, which harbors the central pacemaker, but also in most peripheral tissues. It is believed that the SCN clock entrains the phase of peripheral clocks via chemical cues, such as rhythmically secreted hormones. Here we show that temporal feeding restriction under light–dark or dark–dark conditions can change the phase of circadian gene expression in peripheral cell types by up to 12 h while leaving the phase of cyclic gene expression in the SCN unaffected. Hence, changes in metabolism can lead to an uncoupling of peripheral oscillators from the central pacemaker. Sudden large changes in feeding time, similar to abrupt changes in the photoperiod, reset the phase of rhythmic gene expression gradually and are thus likely to act through a clock-dependent mechanism. Food-induced phase resetting proceeds faster in liver than in kidney, heart, or pancreas, but after 1 wk of daytime feeding, the phases of circadian gene expression are similar in all examined peripheral tissues.

Loss of a circadian adrenal corticosterone rhythm following suprachiasmatic lesions in the rat.

Abstract: The role of vision in neuroendocrine regulation is well-known1, 2, but few data are available on specific visual pathways mediating such functions or their relation to brain centers controlling rhythmic events. Two sets of observations are pertinent to these problems. First, selective ablation of the inferior accessory optic tracts in the rat eliminates the response of the pineal melatonin-forming enzyme, hydroxyindole-Omethyltransferase (HIOMT) to light, without affecting visually guided behavioral responses, whereas section of the primary optic tracts causes a loss of visual behavior with preservation of the pineal HIOMT response to light 3-5. Second, Critchlow 6 has found that lesions in the suprachiasmatic region of the hypothalamus abolish the constant estrous response to light in the female rat, a response that is maintained after section of the primary optic tracts. His observations are of particular interest in view of the recent demonstration of a direct retinohypothalamic projection terminating in the suprachiasmatic nuclei in the rat v. The purpose of the present study was to reinvestigate the role of the central retinal projections in neuroendocrine regulation. In the studies noted above, only prolonged responses to continuous lighting conditions were examined. The experiments reported here were directed toward a different function, the neural regulation of a true circadian rhythm exemplified by the diurnal variation in adrenal corticosterone content1, 6. Two experiments were performed. The subjects for each were female albino rats (Holtzman Co., Madison, Wis.) weighing approximately 180-200 g at the beginning of the experiment. Female rats were used in these experiments because theirdiurnal rhythm in adrenal corticosterone content has a greater amplitude than that of males 6. They were housed in clear plastic cages (6-8 per cage) with free access to food and water. The cages were in racks illuminated by fluorescent lamps (Vita-Lite, Duro-Test Corp.) with a light emission similar to that of natural light. The animals were exposed to approximately 50 ft.-cd of illumination during the 12 h (07.00 to 19.00) the lights were on each day. All surgical procedures were performed under ether anesthesia. The animals were sacrificed on the 21st postoperative day at 4 time points around the clock, 07.09, 13.00, 19.00 and 24.00 hours. Their adrenals were removed and frozen on dry ice prior to subsequent analysis for corticosterone content using a modification of the method of Silber s. The location of each brain lesion was verified by histologic study. In the first experiment 4 groups of animals were used. One was subjected to sham operation and a second to blinding by bilateral orbital enucleation. Visual pathway lesions were placed in the final two groups. In the first of these a lesion was made unilaterally to destroy the optic tract just beyond its emergence from the chiasm (stereotaxic coordinates; anterior 7 ram, lateral 1.5 mm, ventral 2.5 mm below horizontal zero with the tooth bar 5 mm above the ear bars) by passing anodal DC current of 3 mA for 60 sec through an insulated electrode. The eye ipsilateral to the lesion was then removed so that the only intact visual pathways in these animals were the retinohypothalamic projection and one uncrossed primary optic tract. Because of