学术文献库

Mechanical algesia is an important process for the preservation of living organisms, allowing potentially life-saving reflexes or decisions when given body parts are stressed. Yet, its various underlying mechanisms remain to be fully unravelled. Here, we quantitatively discuss how the detection of painful mechanical stimuli by the human central nervous system may, partly, rely on thermal measurements. Indeed, most fractures in a body, including microscopic ones, release some heat, which diffuses in the surrounding tissues. Through this physical process, the thermo-sensitive TRP proteins, that translate abnormal temperatures into action potentials, shall be sensitive to damaging mechanical inputs. The implication of these polymodal receptors in mechanical algesia has been regularly reported, and we here provide a physical explanation for the coupling between thermal and mechanical pain. In particular, in the human skin, we show how the neighbouring neurites of a broken collagen fiber can undergo a sudden thermal elevation that ranges from a fraction to tens of degrees. As this theoretical temperature anomaly lies in the sensibility range of the TRPV3 and TRPV1 cation channels, known to trigger action potentials in the neural system, a degree of mechanical pain can hence be generated.