治疗疼痛 z-bo 2020-10-23 411

　　Pain is an unpleasant feeling that people often encounter in their lives. It is a warning signal that the body is threatened and a special protection function that is indispensable to life. On the other hand, it is a common symptom of various diseases and one of the serious problems that plague human health today. It can also be seen from the poem that a person is in pain and needs the care of the whole family.

　　Pain Loop Research

　　In recent years of research, researchers have gradually discovered that activation of corticostatin interneurons can prevent the development of neuropathic pain; there is a direct causal relationship between BLA-mPFC-PAG- spinal cord pathway disorders, pain perception and emotional components The middle gastrothalamic nucleus (MD), central lateral nucleus (CL) and parafascicular nucleus (PF) are involved in the regulation of pain more clearly; the γ wave oscillation of GABAergic neurons regulates the activities of other neurons in the cortical area related to pain and emotion , And adjust the intensity of nociception through PAG-RVM-spinal axis.

　　The application of emerging technologies to clarify the mechanism of pain is of great help

　　Electrophysiology/optical fiber recording method can confirm the changes of pain-related ion channels. Single-cell sequencing technology can explain the changes in related gene expression after pain occurs. At the same time, based on minimally invasive precision, optogenetics technology has become an essential technology in pain research.

　　In the anterior cingulate cortex, light activation of GABAergic inhibitory neurons greatly reduces acute pain, and activation of excitatory pyramidal neurons using ChR2 significantly increases mechanical sensitivity without affecting inflammation-induced mechanical pain. On the contrary, silencing these neurons with eNpHR3.0 showed the opposite effect, that is, it reversed the inflammation-induced mechanical pain without affecting the underlying mechanical sensitivity. Simultaneously using similar methods to activate central amygdala neurons can lead to increased visceral pain.

　　The serotonergic neurons in the dorsal raphe nucleus are the main source of serotonin input in many brain regions, and ChR2 activation of 5-HA neurons here can lead to reduced mechanical sensitivity in mice, thereby supporting optogenetics to regulate acute The effectiveness of pain.

　　Under neuropathological conditions, selective light activates the layer V neurons of the medial prefrontal cortex (mPFC). In the thermal and mechanical hypersensitivity stimulation model, the neuropathic pain can be reversed. Using the conditional position preference experimental paradigm, mice will avoid rooms that receive blue light-activated mPFC, and choose rooms that are related to yellow light-induced inhibition, indicating that optogenetic regulation of mPFC can also affect the emotional component of neuropathic pain.

　　Oxytocin (OT) is a neuropeptide secreted by the paraventricular (PVN) and supraoptic (SON) nuclei of the hypothalamus. Neurons in these nuclei innervate a large area of the forebrain and release OT from the posterior pituitary. Into the blood. In animal inflammatory pain models, the release of OT induced by ParvOT neurons can inhibit pain and promote analgesia.