Researchers from the Shenzhen Institutes of Advanced Technology (SIAT) of the Chinese Academy of Sciences and their collaborators uncovered answers on chronic stress-induced bone loss.
Previous clinical studies have found that bone mineral density to be much lower in patients with anxiety or depression as compared to those without. The mechanism behind this association was studied and recently published by a team from the Chinese Academy of Sciences.
The scientists found that a central neural circuit from the forebrain to the hypothalamus mediates chronic stress-induced bone loss via the peripheral sympathetic nervous system. Results were published in a paper in the Journal of Clinical Investigation in early September 2020.
A mouse model was used by the research team to identify the neural mechanism underlying chronic stress-induced bone loss. The mice were subjected to episodes of chronic mild stress over a period of four to eight weeks. After which the mice displayed significant behaviours of anxiety. Upon testing, the mice in the group which was exposed to chronic stress had significantly lower bone mineral density as compared to the control group.
Researchers then identified that a population of inhibitory neurons that produce somatostatin in the brain nucleus which are known as the bed nucleus of the stria terminalis in the forebrain were activated. This was especially so in those mice that displayed anxiety behaviour and triggered the transmission of the “anxiety” molecular pathway to the neurons in the ventromedial hypothalamus (VMH).
"Activating the BNST-VMH neural circuit can simultaneously induce anxiety-like behaviors and generate bone loss in the mice, whereas inhibition of this circuit can prevent stress-induced anxiety and bone loss at the same time," said Prof. Yang Fan from SIAT, the co-first and co-corresponding author of the study.
Furthermore, the researchers discovered that glutamatergic neurons in nucleus tractus solitaries (NTS) and the sympathetic system were employed to regulate stress-induced bone loss.
"This study provides a new perspective for the systematic study of the regulatory mechanism of brain homeostasis on metabolism and endocrine function of the body in special environments," said Prof. Wang Liping, Director of the Brain Cognition and Brain Disease Institute of SIAT.