The established function of thyroid stimulating hormone (TSH) is to promote thyroid follicle development and hormone secretion. The osteoporosis associated with hyperthyroidism is traditionally viewed as a secondary consequence of altered thyroid function. We provide evidence for direct effects of TSH on both components of skeletal remodeling, osteoblastic bone formation, and osteoclastic bone resorption, mediated via the TSH receptor (TSHR) found on osteoblast and osteoclast precursors. Even a 50% reduction in TSHR expression produces profound osteoporosis (bone loss) together with focal osteosclerosis (localized bone formation). TSH inhibits osteoclast formation and survival by attenuating JNK/c-jun and NFkappaB signaling triggered in response to RANK-L and TNFalpha. TSH also inhibits osteoblast differentiation and type 1 collagen expression in a Runx-2- and osterix-independent manner by downregulating Wnt (LRP-5) and VEGF (Flk) signaling. These studies define a role for TSH as a single molecular switch in the independent control of both bone formation and resorption.

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The role of the vomeronasal organ (VNO) in the male-induced enhancement of sexual receptivity in ovariectomized estrogen-primed rats was investigated. Removal of the VNO significantly reduced the enhancement of sexual receptivity following mating, as compared with the sham-operated controls. The sham-operated females exhibited a surge of luteinizing hormone (LH) following mating; however, LH release induced by pairing with males was less manifested in the VNO-removed females. This suggests that in female rats, VNO removal impairs the male-induced release of LH-releasing hormone (LHRH). Since LHRH enhances sexual receptivity in ovariectomized estrogen-primed rats, the present results suggest that the increase in sexual receptivity in female rats following mating probably results from a VNO-mediated LHRH release.

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