scholarly journals Propofol inhibits expression of angiotensin II receptor type 2 in dorsal root ganglion neurons

2017 ◽  
Vol 13 (3) ◽  
pp. 867-872
Author(s):  
Bingbing Pan ◽  
Zhigang Cheng ◽  
Gaoyin Kong ◽  
Zongbin Song ◽  
Yunjiao Wang ◽  
...  
2020 ◽  
Vol 18 (10) ◽  
pp. 791-797
Author(s):  
Qiong Xiang ◽  
Jing-Jing Li ◽  
Chun-Yan Li ◽  
Rong-Bo Tian ◽  
Xian-Hui Li

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.


2001 ◽  
Vol 86 (1) ◽  
pp. 241-248 ◽  
Author(s):  
Luz M. Cardenas ◽  
Carla G. Cardenas ◽  
Reese S. Scroggs

The physiological effects of 5HT receptor coupling to TTX-resistant Na+ current, and the signaling pathway involved, was studied in a nociceptor-like subpopulation of rat dorsal root ganglion (DRG) cells (type 2), which can be identified by expression of a low-threshold, slowly inactivating A-current. The 5HT-mediated increase in TTX-resistant Na+ current in type 2 DRG cells was mimicked and occluded by 10 μM forskolin. Superfusion of type 2 DRG cells on the outside with 1 mM 8-bromo-cAMP or chlorophenylthio-cAMP (CPT-cAMP) increased the Na+ current, but less than 5HT itself. However, perfusion of the cells inside with 2 mM CPT-cAMP strongly increased the amplitude of control Na+currents and completely occluded the effect of 5HT. Thus it appears that the signaling pathway includes cAMP. The phosphodiesterase inhibitor 3-isobutyl-l-methylxanthine (200 μM) also mimicked the effect of 5HT on Na+ current, suggesting tonic adenylyl cyclase activity. 5HT reduced the amount of current required to evoke action potentials in type 2 DRG cells, suggesting that 5HT may lower the threshold for activation of nociceptor peripheral receptors. The above data suggest that serotonergic modulation of TTX-resistant Na+channels through a cAMP-dependent signaling pathway in nociceptors may participate in the generation of hyperalgesia.


2014 ◽  
Vol 9 (2) ◽  
pp. 119 ◽  
Author(s):  
Xuegang Luo ◽  
Dan Chen ◽  
Xiaoxin Cheng ◽  
Qilin Cao ◽  
Chunling Fan ◽  
...  

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