Progress in sodium ion channel and pain research

May 8, "Nature - Communications" online journal published a research paper entitled Spidervenom-derivedpeptideinduceshyperalgesiainNav1.7knockoutmicebyactivatingNav1.9channels of the study by the Hunan Normal University, Professor Liu Zhonghua research group and brain sciences and Chinese Academy of sciences innovation intelligence Center of Excellence (Neuroscience Institute), Huazhong University of Science and technology, College of life Science and technology, Liu Jingyu research group collaborationThe study by Nav1.7, Nav1.8, Nav1.9 knockout mouse model in addition, the joint use of patch-clamp technique behavioral analysis found that spider venom HpTx1 inhibiting Nav1.7, activate Nav1.9, but does not affect Nav1.8, Nav1.7 further knockout mice can be recovered in addition to painThis is the first study revealed ganglion neurons in the dorsal root activation and the relationship between three channel may partially compensate for loss of function of Nav1.7 in the action potential in the channel Nav1.9, Nav1.7 is further related to congenital absence of treatment pain provides a new directionhuman feeling pain is subject to various noxious stimuli generatedPain is a defensive mechanism to protect the body from injury, is one kind of the body's internal warning system, but also to promote the healing of damaged tissueHowever Nav1.7 deficits lead to congenital absence of pain, nociceptive stimuli lost their vigilanceBut for the treatment of the disease is a major challengeNav1.7 result in loss of function Congenital pain, studies have shown that Nav1.7 knockout mice leads to an increase of endogenous opioids, naloxone blocks the action of the substance, and thus restore the mouse pain, and no effect in ratsHowever, naloxone act indirectly by reducing the endogenous opioid, it will be accompanied by side effectsTherefore, exploring new treatment Nav1.7 congenital absence of pain-related loss of function of specific targets is even more importantThe first studyobtained by screening polypeptides for the toxin function of Nav1.7 null mice induced pain model generation function, and then found that the toxin can be increased current Nav1.9, Nav1.7 currents but inhibitedBy Nav1.7 knockout mice, Navl.8 knockout mice, Navl.9 knockout mouse model, Nav1.7 / Nav1.8 double knockout mouse model in addition, demonstrated in Navl.9 mouse dorsal root ganglion neurons in effect, revealing the toxin HpTx1 recovery Nav1.7 knockout mice contribution of pain mechanisms and three channels on the action potential (FIGa, b)study for the treatment of the congenital absence of pain associated Nav1.7 provides new strategies and new targets, missing Nav1.7 function for subsequent treatment of patients with congenital absence of drug development Pain It provides a new idea; knockout mice by different discovery Nav1.7, Nav1.8 channels jointly, and a fine adjustment three Navl.9 neuronal excitability, Nav1.9 activation may partially compensate for loss of function Nav1.7 (a in FIG, b); agonists Nav1.9 was first discovered and proved Nav1.9 important role in the transduction of pain signaling pathway pharmacologically (A Biovalley Bioon.com)