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.