Endocrine Abstracts

Photoperiodic time measurement is achieved through a hypothalamic pacemaker that generates a circadian rhythm of photoinducibilty. The presence of light during the photoindicible phase of this rhythm induces photoperiodic responses. Coincidence of light and the photoinducible phase induces increased expression of TSH beta in pars tuberalis cells that results in a local increase in TSH in the adjacent medial basal hypothalamus (MBH). This in turn stimulates local metabolism of T₄ to T₃ in MBH tanycytes by inducing expression of type 2 iodothyronine deiodinase (Dio2). The photoinduced increase in T₃ in the MBH appears to regulate neuropeptide release into the hypophysial portal vasculature by modulating the plasticity of tanycyte end feet surrounding neurosecretory terminals in the median eminence.

Whilst mammals use photoreceptors in their eyes and pineal melatonin to monitor the duration of the daily light period for photoperiodic signalling, birds use extra retinal photoreceptors. The identity of the pathway through which photoperiodic signalling is detected by the avian pars tuberalis is uncertain since circulating melatonin does not control photoperiodically-regulated avian gonadal cycles. However, melatonin appears to be generated locally within the avian MBH in dopaminergic neurones, raising the possibility in birds that photoperiodic signalling within the MBH is transduced by circadian-gated changes in local concentrations of melatonin.

Long days also stimulate pars tuberalis TSH beta and Dio2 in the MBH in the non- photoperiodic mouse. It is unknown what use the mouse makes of photoperiodic information. TSH beta is also present in the human pars tuberalis. Could pars tuberalis TSH beta cells also be providing humans with photoperiodic information? If so how is this information used?