“An unexpected finding of our study is the fact that Flx can function directly on osteoclasts through a pathway that is different from its canonical mode of action,” write the authors in their discussion. “Although cells from the osteoclast lineage express 5HTT and the gene encoding Tph1, osteoclasts derived from mice lacking expression of these proteins respond to Flx similarly to WT [wild type] cells. Thus, at least in mice, Flx acts on these cells independently of the serotonin–5HTT system.”
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Over time, treatment with Flx triggers a brain-serotonin-dependent rise in sympathetic output that increases bone resorption to a level that counteracts the local anti-resorptive effect of Flx. The investigators were able to block this longer-term systemic effect and prevent Flx-induced bone loss by co-treatment with the β-blocker propranolol.
Lara C. Pullen, PhD, is a medical writer based in the Chicago area.
- Ortuño MJ, Robinson ST, Subramanyam P, et al. Serotonin-reuptake inhibitors act centrally to cause bone loss in mice by counteracting a local anti-resorptive effect. Nat Med. 2016 Oct;22(10):1170-1179. doi: 10.1038/nm.4166. Epub 2016 Sep 5.