Noradrenaline depolarization and hyperpolarization mediated by alpha-adrenergic receptors in the soma of dorsal root ganglion neurons

1988 ◽  
Vol 8 (3) ◽  
pp. 144-149 ◽  
Author(s):  
Li Zhi-wang ◽  
Wang A-jing ◽  
Leng Ming ◽  
Yang Xiu-ping
Keyword(s):  
Dorsal Root Ganglion ◽  
Adrenergic Receptors ◽  
Dorsal Root ◽  
Dorsal Root Ganglion Neurons ◽  
Alpha Adrenergic Receptors ◽  
Ganglion Neurons

scholarly journals Adrenergic receptors inhibit TRPV1 activity in the dorsal root ganglion neurons of rats

PLoS ONE ◽  
2018 ◽  
Vol 13 (1) ◽  
pp. e0191032 ◽  
Author(s):  
Yumi Matsushita ◽  
Miki Manabe ◽  
Naoki Kitamura ◽  
Izumi Shibuya
Keyword(s):  
Dorsal Root Ganglion ◽  
Adrenergic Receptors ◽  
Dorsal Root ◽  
Dorsal Root Ganglion Neurons ◽  
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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