However, the output from this signalling system remains to be identified. One of the genes identified on the microarray as differentially expressed between LD and SD rats, and a potential target of triiodothyronine and intermediate between thyroid hormone signalling and GHRH is GALP. GALP was originally discovered as a ligand of galanin receptors in the porcine hypothalamus . GALP distribution in the rat brain is predominantly in neural cell bodies in the hypothalamic ARC, median eminence and infundibular stalk . GALP expression may be regulated by thyroid hormone, given that thyroidectomized rats have been reported as having significantly fewer GALP-expressing cells in the ARC than sham operated controls, and replacement of thyroxine partially reverses this effect . GALP is also regulated by leptin and insulin and is thought to participate in the regulation of reproduction and metabolism and may play a role in growth regulation. GALP can stimulate growth hormone secretion in Rhesus monkey and rat . In addition, recently, a role for GALP in stimulating intracellular calcium concentrations in GHRH neurons in the ARC, but not in NPY or POMC neurons, has been reported . GHRH is the main stimulatory neuropeptide involved in generating and maintaining GH secretion in mammals . Previously we showed that GHRH mRNA levels in the ARC were higher after 28d in LD than SD in the F344 rat and we show here that the SD suppression could be achieved within 3 days. The reciprocal up-regulation of GHRH was Abmole Masitinib observed within 3 days of RWJ 64809 p38 MAPK inhibitor transfer from SD10:14 to LD14:10. GALP however, was found to be expressed in the arcuate nucleus of the F344 rat but did not show higher levels of mRNA expression in LD compared to SD until 14d. Although the GALP mRNA expression seen in LD14:10 rats was also attenuated in melatonin injected LD14:10 rats after 14d, there was no significant difference between LD14:10 and SD10:14 rats at 3 or 14d. At present there is insufficient evidence to invoke GALP as an intermediate between photoperiodically controlled thyroid hormone signalling and GHRH, due to the temporal asynchrony between the changes in GALP and GHRH gene expression, such that GHRH mRNA responses occurred ahead of any changes in GALP mRNA level with either photoperiod or melatonin.