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    Home > Active Ingredient News > Study of Nervous System > Progress has been made in the study of nerve mechanisms that induce bone loss due to stress.

    Progress has been made in the study of nerve mechanisms that induce bone loss due to stress.

    • Last Update: 2020-10-07
    • Source: Internet
    • Author: User
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    On September 10, The Journal of Clinical Research published online a long paper by researchers from the Shenzhen Institute of Advanced Technology of the Chinese Academy of Sciences on the topic of A GABAergic neural circuit in the ventromedial hypothalamus media direct-induced bone loss ("GABA-induced bone loss in the inner region of the hypothalamus").
    the study found that a neural loop consisting of the bed nucleus of the stria terminalis (BNST) to the ventromedial hypothalamus (VMH) to the nucleus tractus solitaries (NTS) regulates the loss of bone by regulating peripheral sensory nervous system activity.
    with the development of modern society and the acceleration of the pace of life, people's stress increased significantly.
    chronic stress can lead to a variety of diseases in the body, including mood disorders, osteoporosis and metabolic abnormalities.
    In the 1970s and 1980s, clinical studies found that patients with anxiety or depression had lower bone density than normal, suggesting that stress-related anxiety may be closely related to bone loss, but biological mechanisms are unclear.
    In space medicine, the traditional view is that the loss of astronauts' bones is caused by the loss of gravity in the outer space environment, but recent studies have found that astronauts still have persistent loss of bone mass even after long periods of exercise, which suggests chronic stress caused by special environments such as confined isolation or aggravates the loss of astronauts' bones.
    the functional state of the brain under stress may have a sustained negative effect through the external peripheral metabolism of the nervous system, however, the biological mechanism of this effect is not yet known.
    in order to analyze its biological mechanism in depth, Shenzhen Advanced Institute, in cooperation with the China Astronaut Research and Training Center, has made progress in the field of stress-induced bone loss neurodevelitic analysis through six years of research.
    human trials, the team found that confined spaces can lead to a significant increase in anxiety and bone loss symptoms in subjects, confirming the direct correlation between stress and bone loss.
    researchers used an unpredictable model of chronic mild stress mice (Unpredictable chronic mild-model, UCMS) to analyze the neural mechanisms that cause bone loss caused by stress stress.
    results showed that mice stimulated by chronic stress showed significant anxiety-like behavior, accompanied by bone loss.
    by combining neuro-loop tradistic technology, photogenetic/drug genetic regulation techniques, electrophysiological and bone analysis, the researchers analyzed a SOM neuron (Somatostatin) from the BNST nucleology. growth inhibitors) and the SF-1 neurons of the VMH nucleus (steroidogenic factor-1, steroid-producing factor 1) form a neural loop, which regulates Vglut2 neurons in the lone beam nucleus NTS (vesicular glutamate transporter-2, II. Type vesicle membrane glutamate transporter) and peripheral intersecting nerve activity to regulate chronic stress-induced bone loss symptoms: when animals are in an anxious state, BNST nucleus SOM neurons are activated, thereby inhibiting SF-1 neuron activity in VMH; these inhibited SF-1 neurons reduce the excitability of Vglut2 neurons in downstream NTS, causing increased peripheral sensory neuron activity. To secrete more norepinephrine (Norepinephrine, NE), which inhibits bone-forming and promotes bone-breaking by acting on beta-2 subjects on bone cells and induces bone loss.
    this study provides new ideas for understanding the neural mechanisms of the brain that regulate the function of the exosome, and provides a new research perspective for the study of the mechanism of the brain's steady state to regulate the metabolism and endocrine function of the body in confined/isolated environments.
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