Aims: 

A fundamental property of circadian rhythms is the ability to entrain to different light cycles and shape behaviour. Seasonality in both daily locomotor activity patterns and reproduction is manifest in mammals, with melatonin as an important seasonal signal controlled by the central biological clock. The purpose of this study was to examine the mechanisms of seasonal encoding by circadian pacemaker neurons in the suprachiasmatic nuclei of the hypothalamus (SCN), the brain's central biological clock.

Methods: 

Transgenic mice harboring a short half-life Per1: GFP clock gene reporter were kept in wheel-running cages in one of three photoperiodic cycles: short-photoperiod (8:16), control (12:12) and long-photoperiod (16:8). 200u coronal slices of the SCN were taken from each mouse for time-lapse laser-scanning confocal microscopy of 4 circadian cycles in vitro. The organization of the mouse SCN Per1 expression was observed at the cellular level by imaging GFP fluorescence and correlated with previous running wheel activity on the different photoperiods.

Results: 

Both the waveform of Per1 expression within individual SCN neurons and the distribution of individual neuronal peak times shaped the activity of the SCN clock network in response to photoperiod. In addition, we noted significant "after effects" on cellular period in vitro of the long and short light cycles and peak-to-peak period inconsistencies in individual neurons that suggest lability of the constituent cellular oscillators of the SCN at the molecular level.

Conclusions: 

Our results suggest that both intra-neuronal molecular mechanisms and inter-neuronal coupling are involved in encoding seasonal changes by the biological clock.