Mécanismes de plasticité structurale associés à la synchronisation photique de l'horloge circadienne au sein du noyau suprachiasmatique

Apr 11, 2009Journal de la Societe de biologie

How the brain's internal clock changes structure to sync with light signals

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Abstract

The rhythmic expression of glial fibrillary acidic protein (GFAP) in the suprachiasmatic nucleus (SCN) is disrupted under constant darkness.

The mammalian circadian clock is primarily regulated by the light/dark cycle, which synchronizes its timing to the 24-hour astronomical day.
Structural changes in the SCN's neuronal-glial network occur in response to light exposure, affecting the coordination of circadian rhythms.
Two main types of neurons in the SCN, those producing vasoactive intestinal peptide (VIP) and arginine-vasopressin (AVP), play critical roles in processing and communicating light signals.
Glucocorticoid hormones are essential for maintaining the normal amplitude of the GFAP rhythm, suggesting their role in regulating astrocytic changes in the SCN.
Daily fluctuations in glucocorticoids may help the circadian system adapt to varying light conditions, supporting the synchronization of the clock.

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The mammalian circadian clock, whose central component is located in the suprachiasmatic nucleus of the hypothalamus (SCN), orchestrates rhythmic events in metabolism, physiology and behavior. Adaptation of the organism to its environment requires precise adjustment of the clock to the 24 h astronomical time, primarily by the light/dark cycle. Photic synchronization acts on both the molecular loops which trigger circadian oscillations and the phasing of the multiple SCN cellular oscillators whose coordination permits elaboration of the rhythmic message that will be distributed throughout the organism. It is concomitant with structural plastic events characterized by day/night rearrangements of the SCN neuronal-glial network. The two main sources of SCN efferents, namely the VIP (vasoactive intestinal peptide)-synthesizing neurons which are major integrators of photic signals and the AVP (arginine-vasopressin)-synthesizing neurons which are known to importantly contribute to conveying rhythmic messages to brain targets, are involved in these mechanisms. Over the light/dark cycle, they indeed undergo ultrastructural changes in the extent of their membrane coverage by glial, axon terminal and/or somato-dendritic elements. These structural rearrangements appear to be dependent on light entrainment, as the rhythmic expression in SCN of glial fibrillary acidic protein (GFAP), a marker for brain astrocytes whose changing expression has proved to be a reliable index of neuronal-glial plasticity, is disrupted under constant darkness. Glucocorticoid hormones, which are known as important endocrine outputs of the clock, are required to maintain amplitude of the SCN GFAP rhythm to normal values, indicating that they modulate astrocytic plasticity within the SCN and, therefore, nycthemeral changes of the configuration of its neuronal-glial network. The view that such plastic events may subserve synchronization of the clock to the light-dark cycle is reinforced by other data showing that the daily fluctuations of circulating glucocorticoids actually are involved in modulation of light effects, contributing to the resistance of the circadian timing system to variations of the photoperiod. It is thus proposed that the capacity of the clock to integrate cyclic variations of the environment rely on the inherent capacity of the SCN to undergo neuronal-glial plasticity.

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Mécanismes de plasticité structurale associés à la synchronisation photique de l'horloge circadienne au sein du noyau suprachiasmatique

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