2.Treatment of C severe fracture and dislocation combined with cervical spinal cord injury by one stage reduction and internal fixation with anterior posterior approaches : a case report.
Jian-Quan CHEN ; Mao-Shui CHEN ; Bo ZHANG ; Hao-Bin CENG ; Luo-Qi MAI ; Wei-Yi XIA ; Hao LI
China Journal of Orthopaedics and Traumatology 2020;33(2):154-157
3. Tweety-Homolog 1 Facilitates Pain via Enhancement of Nociceptor Excitability and Spinal Synaptic Transmission
Wen-Juan HAN ; Hai-Ning WU ; Hua HAN ; Wen-Juan HAN ; Sui-Bin MA ; Rou-Gang XIE ; Zhen-Zhen LI ; Fei WANG ; Sheng-Xi WU ; Ceng LUO ; Wen-Bin WU ; Fu-Dong WANG ; Xiu-Li CAO ; Min-Hua ZHENG ; Dong-Hao WANG
Neuroscience Bulletin 2021;37(4):478-496
Tweety-homolog 1 (Ttyh1) is expressed in neural tissue and has been implicated in the generation of several brain diseases. However, its functional significance in pain processing is not understood. By disrupting the gene encoding Ttyh1, we found a loss of Ttyh1 in nociceptors and their central terminals in Ttyh1-deficient mice, along with a reduction in nociceptor excitability and synaptic transmission at identified synapses between nociceptors and spinal neurons projecting to the periaqueductal grey (PAG) in the basal state. More importantly, the peripheral inflammation-evoked nociceptor hyperexcitability and spinal synaptic potentiation recorded in spinal-PAG projection neurons were compromised in Ttyh1-deficient mice. Analysis of the paired-pulse ratio and miniature excitatory postsynaptic currents indicated a role of presynaptic Ttyh1 from spinal nociceptor terminals in the regulation of neurotransmitter release. Interfering with Ttyh1 specifically in nociceptors produces a comparable pain relief. Thus, in this study we demonstrated that Ttyh1 is a critical determinant of acute nociception and pain sensitization caused by peripheral inflammation.
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