Detection of thyroid hormone receptors in the olfactory system and brain of wild masu salmon,Oncorhynchus masou (Brevoort), during smolting by in vitro autoradiography

Thyroid hormone regulates a number of physiological functions during smolting in salmonids. However, the target sites and roles of thyroid hormone in the central nervous system (CNS) are not known in detail. We detected thyroid hormone-specific binding sites (i.e. thyroid hormone receptors) in the olfactory epithelium and the brain (the olfactory bulb, the telencephalon, the mid-brain and the cerebellum) of wild masu salmon, Oncor- hynchus masou (Brevoort), during smolting by means of in vitro autoradiography with frozen sections. A saturation experiment with the brain indicated the presence of a single class of binding sites of high affinity. T3-specific binding was detected in the olfactory epithelium and in all regions of the brain except the olfactory bulb. The T3-specific binding value in the olfactory epithelium was higher than in all other regions of the brain. This binding value in the olfactory epithelium increased at the full-smolt stage. The presence of thyroid hormone receptors in various regions of the CNS suggests that thyroid hormone plays an important role in the functional change in the brain and the olfactory epithelium during smolting.     

Central somatostatin-somatostatin receptor 2 signaling mediates lactational suppression of luteinizing hormone release via the inhibition of glutamatergic interneurons during late lactation in rats

Reproductive function is suppressed during lactation owing to the suckling-induced suppression of the kisspeptin gene (Kiss1) expression in the arcuate nucleus (ARC) and subsequent suppression of luteinizing hormone (LH) release. Our previous study revealed that somatostatin (SST) neurons mediate suckling-induced suppression of LH release via SST receptor 2 (SSTR2) in ovariectomized lactating rats during early lactation. This study examined whether central SST-SSTR2 signaling mediates the inhibition of ARC Kiss1 expression and LH release in lactating rats during late lactation and whether the inhibition of glutamatergic neurons, stimulators of LH release, is involved in the suppression of LH release mediated by central SST-SSTR2 signaling in lactating rats. A central injection of the SSTR2 antagonist CYN154806 (CYN) significantly increased ARC Kiss1 expression in lactating rats on day 16 of lactation. Dual in situ hybridization revealed that few ARC Kiss1-positive cells co-expressed Sstr2, and some of the ARC Slc17a6 (a glutamatergic neuronal marker)-positive cells co-expressed Sstr2. Furthermore, almost all ARC Kiss1-positive cells co-expressed Grin1, a subunit of N-methyl-D-aspartate (NMDA) receptors. The numbers of Slc17a6/Sstr2 double-labeled and Slc17a6 single-labeled cells were significantly lower in lactating dams than in non-lactating rats whose pups had been removed after parturition. A central injection of an NMDA antagonist reversed the CYN-induced increase in LH release in lactating rats. Overall, these results suggest that central SST-SSTR2 signaling, at least partly, mediates the suppression of ARC Kiss1 expression and LH release by inhibiting ARC glutamatergic interneurons in lactating rats.