TY  - JOUR
PY  - 2023//
TI  - Chronic salmon calcitonin exerts an antidepressant effect via modulating the p38 MAPK signaling pathway
JO  - Frontiers in molecular neuroscience
A1  - Zhu, Wenhui
A1  - Li, Weifen
A1  - Jiang, Jian
A1  - Wang, Dilong
A1  - Mao, Xinliang
A1  - Zhang, Jin
A1  - Zhang, Xunzhi
A1  - Chang, Jinlong
A1  - Yao, Peijia
A1  - Yang, Xiuyan
A1  - Da Costa, Clive
A1  - Zhang, Ying
A1  - Yu, Jiezhong
A1  - Li, Huiliang
A1  - Li, Shupeng
A1  - Chi, Xinjin
A1  - Li, Ningning
SP  - e1071327
EP  - e1071327
VL  - 16
IS  - 
N2  - Depression is a common recurrent psychiatric disorder with a high lifetime prevalence and suicide rate. At present, although several traditional clinical drugs such as fluoxetine and ketamine, are widely used, medications with a high efficiency and reduced side effects are of urgent need. Our group has recently reported that a single administration of salmon calcitonin (sCT) could ameliorate a depressive-like phenotype via the amylin signaling pathway in a mouse model established by chronic restraint stress (CRS). However, the molecular mechanism underlying the antidepressant effect needs to be addressed. In this study, we investigated the antidepressant potential of sCT applied chronically and its underlying mechanism. In addition, using transcriptomics, we found the MAPK signaling pathway was upregulated in the hippocampus of CRS-treated mice. Further phosphorylation levels of ERK/p38/JNK kinases were also enhanced, and sCT treatment was able only to downregulate the phosphorylation level of p38/JNK, with phosphorylated ERK level unaffected. Finally, we found that the antidepressant effect of sCT was blocked by p38 agonists rather than JNK agonists. These results provide a mechanistic explanation of the antidepressant effect of sCT, suggesting its potential for treating the depressive disorder in the clinic.<p />  <p>Language: en</p>
LA  - en
SN  - 1662-5099
UR  - http://dx.doi.org/10.3389/fnmol.2023.1071327
ID  - ref1
ER  -