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。 Distribution of excitable neurons and inhibitory neurons in the LPBN brain region guang activates excitable neurons in the LPBN brain region
pain is a protective response developed by living organisms and is essential for the survival of living organisms. But pathological pain, such as nerve pain, causes great pain to the patient and loses its meaning to the protection of organisms. A major feature of pain is its unpleasant emotional response, and different individuals experience pain with the same injury-stimulating pain.
recently, Duan Shumin, dean of zhejiang University's School of Brain Science and Brain Medicine and a member of the Chinese Academy of Sciences, revealed local neural loop door-controlled nerve pain in the arm-side nucleus. The results were published in nature-newsletter on November 25. This study is not only of great significance for understanding the pathogenesis of nerve pain, but also provides an important new target for clinical intervention of nerve pain.
Duan Shumin told China Science Daily that previous studies of pain have focused on the spinal cord level, and the classic theory of pain control holds that the spinal cord has a pain-gateing system formed by inhibitory neurons, and that neuro-injury and other pathological conditions impair the function of inhibitory neurons in the spinal cord, resulting in persistent pain and pain allergies. However, brain damage above the spinal cord level can also produce neuropathic pain, suggesting that there is a higher central level of pain gateing mechanism.
the outer arm bypass (LPBN) of the brain bridge is thought to be a relay station for the spinal cord to transmit pain information to the brain, where the message to the amygdala in the brain causes an emotional response to pain.
" and our study shows that LPBN, while transmitting pain information, also has an active regulatory effect on pain information. In particular, GABA, which accounts for only 10% of neurons, does not affect physiological pain, but has a key gating effect on neuropathic pain (including sensory and emotional responses) caused by excessive excitement of glutamate neurons. These results suggest that LPBN excitability-inhibition of balance disorders is a key factor in the production of neuropathic pain, and that LPBN is another key gate-controlled center for neuropathic pain outside the spinal cord. Duan Shumin said.
researchers built a neuropathic pain model using phosphedal nerve (CPN) ligation after a large number of excitable neurons in the outer arm bypass (LPBN) brain region were activated, and inhibitory neurons did not show this apparent activation. After injecting calcium ion indicators into the LPBN brain region of tool mice labeled with excitable neurons, fiber-optic calcium imaging technology found that neuropathic pain was activated in large numbers. These results suggest that excitable neurons in the LPBN brain region may encode key information about nerve pain.
To further determine the role of excitable neurons in the LPBN brain region, the researchers activated the excitation neurons in the LPBN brain region through photogenetic techniques, which can obviously cause mechanical pain hypersensitivity, as shown by reducing the latent time of foot reflexes in mice in thermal stimulation experiments, and effectively alleviating pain symptoms after light inhibits excitation neurons in the brain region in neuropathic pain models.
that although only about 10% of inhibitory neurons are activated in the neuropathic pain model, there is little difference from the fake surgical group. It seems that inhibitory neurons do not work, but in light activation LPBN brain region inhibitory neurons, actually can play a role in pain relief. Inhibiting inhibitory neurons in the brain region can cause mechanical pain hypersensitivity.
researchers used viral tools to reveal a direct synhapus connection between LPBN brain region inhibitory neurons and excitable neurons in that brain region. Subsequent electrophysiological experiments did prove that local inhibitory neurons inhibited the activity of excitable neurons. It is shown that there is local neuro-micro-loop regulation of neurogenic pain information in the LPBN brain region.
results reveal that the LPBN brain region not only serves as a relay station for transmitting injury signals from the spinal cord to a higher centrality, but also actively participates in the development of neuropathic pain. (Source: Cui Xueqin, China Science Daily)
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