The tau mutation in the Syrian hamster alters the photoperiodic responsiveness of the gonadal axis to melatonin signal frequency

This study investigated the role of the circadian timing system (CTS) in photoperiodic time measurement by examining the response of the tau mutant hamster to programmed infusions of melatonin. The mutation is a single Mendelian gene defect which accelerates circadian period from 24 h in the wild-type (WT) to 20 h in the homozygote. If the CTS does not contribute to the photoperiodic interpretation of the melatonin signal, then the tau mutation would not influence photoperiodic responses of pinealectomised (PX) animals to systemic infusions of melatonin of programmed frequency and duration. Previous studies have shown that infusion of PX, WT animals with melatonin (10 h) once every 20, 24 or 25 h, mimics short-daylengths and causes gonadal involution. More (25 h) frequent signals are ineffective. In this study, taus which received melatonin (10 h) once every 16 or 20 h exhibited significant gonadal atrophy relative to saline controls, whereas infusions of melatonin every 24 or 28 h were ineffective. Serum concentrations of LH and PRL were also significantly reduced in both the 16 and 20 h, but not 24 and 28 h groups. The tau mutant hamster may therefore respond to a different and higher range of melatonin signal frequencies than those reported for WTs. The 4 h shift in the frequency-response function correlates with the altered circadian period and suggests that the CTS contributes to the photoperiodic interpretation of a series of melatonin signals.