The 24-h (circadian) timing system has the essential task of anticipating daily recurring changes in the environment (day/night) to find the best time for each molecular and cellular process. It is organized hierarchically, with a master pacemaker in the hypothalamic suprachiasmatic nucleus (SCN), which is able to perceive environmental light and tell the body what time is it. Unfortunately, our modern 24/7 lifestyle demands exposure to artificial light all night, people working in night-shifts, travelling across time zones or spending several night hours in front of screens, reducing the ability of the circadian system to anticipate those changes.

Such circadian disruptive environment during pregnancy has been correlated to poor neurodevelopmental outcomes in animal models and human night-shift and jet-lag studies. We have shown in mice and pre-term infants, that when maternal circadian homeostasis is disrupted by exposure to glucocorticoids at the wrong time of day (morning in mice and evening in humans), the offspring show a higher vulnerability to develop behavioral disorders later in life. Our mechanistic studies showed for the first time, a decisive role of the fetal clock before birth, challenging the traditional view on the clock being immature and non-functional.

In this introductory talk I will present the lab and our main aim: to understand mechanistically the development of the central circadian pacemaker in mice and humans. I will share preliminary data and the experimental approaches we are going to use to investigate: HOW this remarkable brain circuit assemble and maturate, WHEN does it become functional to give the time to the rest of the body and WHAT is the influence of the early environment in the whole process