Shift working is now common practice, but surprisingly little is known about its affect at the physiological and neurobiological level. Human beings have evolved internal biological rhythms that are adapted to a night-day cycle - circadian rhythm - but these can be disrupted by artificial lighting and long-haul flights. However, the greatest disruption to the synchronisation of the body's internal rhythm is caused by shift working. Under normal conditions the body's internal clocks are controlled by a central pacemaker known as the suprachiasmatic nucleus (SCN) that is located in the hypothalamus region of the brain. The SCN synchronises certain behavioural and physiological responses according to specific times of day. This synchronisation enables an individual to operate at an optimum physiological and mental level. Loss of synchronisation due to shift working can lead to an abnormal physiological response such as obesity, reduced mental ability and an increase in disease. Researchers from the Clockwork project have developed a comprehensive model for shift work using mice, which can describe the internal desynchronisation between the SCN and hormonal rhythms. The mice have been kept at different shift work schedules. Under normal light-dark cycles the rodents were active and feeding during the dark cycle, while SCN activity was synchronised with the light. Under shift work conditions feeding and forced activity were carried out in three shifts over the LD cycle. Project partners have studied the central nervous system and SCN of the mice and their metabolism and physiology following exposure to the different work schedules. Scientists also investigated rhythms in the peripheral organs of the mice and their behaviour and mental performance. Findings revealed that the LD cycle and the mice's metabolism were linked. Mice that were normally active during the night and sleeping during the day became active in the day and sleeping at night. This was not due to the central circadian clock (SCN) changing its pattern of activity, but due to its loss of influence on a, yet unknown, circadian pacemaker that drives activity.