The Effects of pH on Beta-Endorphin and Morphine Inhibition of Calcium Transients in Dorsal Root Ganglion Neurons

2006 ◽  
Vol 7 (7) ◽  
pp. 488-499 ◽  
Author(s):  
Irina Vetter ◽  
Daniel Kapitzke ◽  
Siobhan Hermanussen ◽  
Gregory Raymond Monteith ◽  
Peter John Cabot
Keyword(s):  
Dorsal Root Ganglion ◽  
Dorsal Root ◽  
Dorsal Root Ganglion Neurons ◽  
Calcium Transients ◽  
Beta Endorphin ◽  
Effects Of Ph ◽  
Ganglion Neurons

scholarly journals Reply to “TRPA1-dependent calcium transients and CGRP release in DRG neurons require extracellular calcium”

2020 ◽  
Vol 219 (6) ◽  
Author(s):  
Bing Liu ◽  
Muhammad Younus ◽  
Suhua Sun ◽  
Yiman Li ◽  
Yuan Wang ◽  
...  
Keyword(s):  
Dorsal Root Ganglion ◽  
Intracellular Calcium ◽  
Dorsal Root ◽  
Extracellular Calcium ◽  
Dorsal Root Ganglion Neurons ◽  
Calcium Transients ◽  
Drg Neurons ◽  
Cgrp Release ◽  
Ganglion Neurons

In this issue, Gebhardt et al. (2020. J. Cell Biol.https://doi.org/10.1083/jcb.201702151) express interest in our recently published work (Shang et al. 2016. J. Cell Biol.https://doi.org/10.1083/jcb.201603081). Here, we would like to address their concerns regarding the lysosomal TRPA1-mediated intracellular calcium transients in dorsal root ganglion neurons.

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.

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