Abstract
In most species, self-sustained molecular clocks regulate 24-h rhythms of behavior and physiology. In mammals, a circadian pacemaker residing in the hypothalamic suprachiasmatic nucleus (SCN) receives photic signals from the retina and synchronizes subordinate clocks in non-SCN tissues. The emergence of circadian rhythmicity during development has been extensively studied for many years. In mice, neuronal development in the presumptive SCN region of the embryonic hypothalamus occurs on days 12–15 of gestation. Intra-SCN circuits differentiate during the following days and retinal projections reach the SCN, and thus mediate photic entrainment, only after birth. In contrast the genetic components of the clock gene machinery are expressed much earlier and during midgestation SCN explants and isolated neurons are capable of generating molecular oscillations in culture. In vivo metabolic rhythms in the SCN, however, are observed not earlier than the 19th day of rat gestation, and rhythmic expression of clock genes is hardly detectable until after birth. Together these data indicate that cellular coupling and, thus, tissue-wide synchronization of single-cell rhythms, may only develop very late during embryogenesis. In this mini-review we describe the developmental origin of the SCN structure and summarize our current knowledge about the functional initiation and entrainment of the circadian pacemaker during embryonic development.
Highlights
Endogenous circadian clocks facilitate the adaptation of behavior and physiology to the 24-h rhythm of day and night
In vivo metabolic rhythms in the suprachiasmatic nuclei (SCN), are observed not earlier than the 19th day of rat gestation, and rhythmic expression of clock genes is hardly detectable until after birth. Together these data indicate that cellular coupling and, tissue-wide synchronization of single-cell rhythms, may only develop very late during embryogenesis. In this mini-review we describe the developmental origin of the SCN structure and summarize our current knowledge about the functional initiation and entrainment of the circadian pacemaker during embryonic development
While the structural development of the SCN is relatively well understood, the question whether endogenous circadian www.frontiersin.org rhythmicity in the SCN develops before birth is still matter of debate and studies based on SCN output or clock gene expression in the SCN provide different results
Summary
Endogenous circadian clocks facilitate the adaptation of behavior and physiology to the 24-h rhythm of day and night. The circadian timing is organized by pacemaker cells in the hypothalamic suprachiasmatic nuclei (SCN). This SCN master clock is reset by photic time cues, or Zeitgebers, perceived through the retina and transmitted via the retino-hypothalamic tract (RHT). The rat SCN is derived from the neuroepithelium of the preoptic recess of the third ventricle and becomes discernable as a discrete structure at embryonic day E17 (Altman and Bayer, 1978b). In the hamster SCN, radial glial cells start to develop at E8 and appear at high density in the SCN at E13. At post-natal day 0 (P0), the density of these cells in the hamster SCN is drastically reduced and by P5 most of them are replaced by neurons. ACTIVATION OF SCN MARKER GENE EXPRESSION The neuropeptides vasopressin (AVP) and vasoactive intestinal polypeptide (VIP) are strongly expressed in the SCN and contribute to its role as circadian pacemaker
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