scholarly journals Effect of nerve injury on the number of dorsal root ganglion neurons and autotomy behavior in adult Bax-deficient mice

2017 ◽  
Vol Volume 10 ◽  
pp. 2079-2087 ◽  
Author(s):  
Chuang Lyu ◽  
Gong-Wei Lyu ◽  
Aurora Martinez ◽  
Tie-Jun Shi
Keyword(s):  
Dorsal Root Ganglion ◽  
Nerve Injury ◽  
Dorsal Root ◽  
Dorsal Root Ganglion Neurons ◽  
Ganglion Neurons ◽  
Deficient Mice

Somatostatin Type 2 Receptor Antibody Enhances Mechanical Hyperalgesia in the Dorsal Root Ganglion Neurons after Sciatic Nerve-pinch Injury: Evidence of Behavioral Studies and Bax Protein Expression

2020 ◽  
Vol 18 (10) ◽  
pp. 791-797
Author(s):  
Qiong Xiang ◽  
Jing-Jing Li ◽  
Chun-Yan Li ◽  
Rong-Bo Tian ◽  
Xian-Hui Li
Keyword(s):  
Sciatic Nerve ◽  
Dorsal Root Ganglion ◽  
Nerve Injury ◽  
Dorsal Root ◽  
Underlying Mechanism ◽  
Dorsal Root Ganglion Neurons ◽  
Mechanical Hyperalgesia ◽  
Bax Protein ◽  
Ganglion Neurons

Background: Our previous study has indicated that somatostatin potently inhibits neuropathic pain through the activation of its type 2 receptor (SSTR2) in mouse dorsal root ganglion and spinal cord. However, the underlying mechanism of this activation has not been elucidated clearly Objective: The aim of this study is to perform the pharmacological studies on the basis of sciatic nerve-pinch mice model and explore the underlying mechanism involving SSTR2. Methods: On the basis of a sciatic nerve-pinch injury model, we aimed at comparing the painful behavior and dorsal root ganglion neurons neurochemical changes after the SSTR2 antibody (anti- SSTR2;5μl,1μg/ml) administration in the mouse. Results: After pinch nerve injury, we found that the mechanical hyperalgesia and severely painful behavior (autotomy) were detected after the application of SSTR2 antibody (anti-SSTR2; 5μl, 1μg/ml) on the pinch-injured nerve. The up-regulated phosphorylated ERK (p-ERK) expression and the apoptotic marker (i.e., Bax) were significantly decreased in DRGs after anti-SSTR2 treatment. Conclusion: The current data suggested that inhibitory changes in proteins from the apoptotic pathway in anti-SSTR2-treated groups might be taking place to overcome the protein deficits caused by SSTR2 antibody and supported the new therapeutic intervention with SSTR2 antagonist for neuronal degeneration following nerve injury.

scholarly journals Positive Regulatory Domain I–binding Factor 1 Mediates Peripheral Nerve Injury–induced Nociception in Mice by Repressing Kv4.3 Channel Expression

2020 ◽  
Author(s):  
Cunjin Wang ◽  
Yuchen Pan ◽  
Wenwen Zhang ◽  
Ying Chen ◽  
Chuhan Li ◽  
...  
Keyword(s):  
Dorsal Root Ganglion ◽  
Peripheral Nerve ◽  
Nerve Injury ◽  
Peripheral Nerve Injury ◽  
Dorsal Root ◽  
Thermal Hyperalgesia ◽  
Dorsal Root Ganglion Neurons ◽  
Channel Expression ◽  
Mouse Dorsal Root Ganglion ◽  
Ganglion Neurons

Background The transcriptional repressor positive regulatory domain I–binding factor 1 (PRDM1) is expressed in adult mouse dorsal root ganglion and regulates the formation and function of peripheral sensory neurons. The authors hypothesized that PRDM1 in the dorsal root ganglion may contribute to peripheral nerve injury–induced nociception regulation and that its mechanism may involve Kv4.3 channel transcriptional repression. Methods Nociception was induced in C57BL/6 mice by applying chronic constriction injury, complete Freund’s adjuvant, or capsaicin plantar injection. Nociceptive response was evaluated by mechanical allodynia, thermal hyperalgesia, cold hyperalgesia, or gait analysis. The role of PRDM1 was evaluated by injection of Prdm1 knockdown and overexpression adeno-associated viruses. The interaction of PRDM1 at the Kv4.3 (Kcnd3) promoter was evaluated by chromatin immunoprecipitation assay. Excitability of dorsal root ganglion neurons was evaluated by whole cell patch clamp recordings, and calcium signaling in spinal dorsal horn neurons was evaluated by in vivo two-photon imaging. Results Peripheral nerve injury increased PRDM1 expression in the dorsal root ganglion, which reduced the activity of the Kv4.3 promoter and repressed Kv4.3 channel expression (injured vs. uninjured; all P < 0.001). Knockdown of PRDM1 rescued Kv4.3 expression, reduced the high excitability of injured dorsal root ganglion neurons, and alleviated peripheral nerve injury–induced nociception (short hairpin RNA vs. Scram; all P < 0.05). In contrast, PRDM1 overexpression in naive mouse dorsal root ganglion neurons diminished Kv4.3 channel expression and induced hyperalgesia (PRDM1 overexpression vs. control, mean ± SD; n = 13; all P < 0.0001) as evaluated by mechanical allodynia (0.6 ± 0.3 vs. 1.2 ± 0.2 g), thermal hyperalgesia (5.2 ± 1.3 vs. 9.8 ± 1.7 s), and cold hyperalgesia (3.4 ± 0.5 vs. 5.3 ± 0.6 s). Finally, PRDM1 downregulation in naive mice reduced the calcium signaling response of spinal dorsal horn neurons to thermal stimulation. Conclusions PRDM1 contributes to peripheral nerve injury–induced nociception by repressing Kv4.3 channel expression in injured dorsal root ganglion neurons. Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New

Gadd45a protects against cell death in dorsal root ganglion neurons following peripheral nerve injury

2011 ◽  
Vol 89 (5) ◽  
pp. 689-699 ◽  
Author(s):  
Chung-Ren Lin ◽  
Chien-Hui Yang ◽  
Chiu-En Huang ◽  
Chih-Hsien Wu ◽  
Yi-Shen Chen ◽  
...  
Keyword(s):  
Cell Death ◽  
Dorsal Root Ganglion ◽  
Peripheral Nerve ◽  
Nerve Injury ◽  
Peripheral Nerve Injury ◽  
Dorsal Root ◽  
Dorsal Root Ganglion Neurons ◽  
Ganglion Neurons

Differential action potentials and firing patterns in injured and uninjured small dorsal root ganglion neurons after nerve injury

2004 ◽  
Vol 1009 (1-2) ◽  
pp. 147-158 ◽  
Author(s):  
Xu-Feng Zhang ◽  
Chang Z Zhu ◽  
Rama Thimmapaya ◽  
Won S Choi ◽  
Prisca Honore ◽  
...  
Keyword(s):  
Dorsal Root Ganglion ◽  
Nerve Injury ◽  
Action Potentials ◽  
Dorsal Root ◽  
Dorsal Root Ganglion Neurons ◽  
Firing Patterns ◽  
Ganglion Neurons ◽  
Differential Action
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