Salmon Calcitonin Exerts an Antidepressant Effect by Activating Amylin Receptors

Jiang, Jian; Ju, Jun; Luo, Lun; Song, Ze; Liao, Huanquan; Yang, Xiuyan; Wei, Shoupeng; Wang, Dilong; Wenhui, Zhu; Chang, Jinlong; Ma, Jien; Hu, Hao; Yu, Jie‐Zhong; Wang, Huiqing; Hou, Sheng T.; Li, Shupeng; Li, Hui‐Liang; Li, Ningning

doi:10.3389/fphar.2022.826055

Cited by 5 publications

(8 citation statements)

References 48 publications

(62 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Depression is a common debilitating neuropsychiatric disorder with an increased incidence year on year (Hammen, 2018). Our group has recently demonstrated that a single administration of sCT could ameliorate a depressive-like phenotype probably via the amylin signaling pathway (Jiang et al, 2022). The potential role of the calcitonin-AMYR axis in depression has been delineated by exploiting both agonists (e.g., sCT) and inhibitors/antagonists of AMYR (e.g., AC187; Hay et al, 2005;Jiang et al, 2022).…”

Section: Discussionmentioning

confidence: 99%

“…Our group has recently demonstrated that a single administration of sCT could ameliorate a depressive-like phenotype probably via the amylin signaling pathway (Jiang et al, 2022). The potential role of the calcitonin-AMYR axis in depression has been delineated by exploiting both agonists (e.g., sCT) and inhibitors/antagonists of AMYR (e.g., AC187; Hay et al, 2005;Jiang et al, 2022). However, the mechanism of its long-term action remains largely unclear.…”

Section: Discussionmentioning

confidence: 99%

“…After being acclimated to the facility for a week, mice were subject to the procedures of CRS as previously described (Jiang et al, 2022). In brief, mice were restrained in flexible cylindrical plastic tubes which were fitted to allow them to breathe.…”

Section: Chronic Restraint Stress Modelmentioning

confidence: 99%

“…sCT (Tocris Bioscience, Bristol, United Kingdom) was diluted in sterile 0.9% saline and injected subcutaneously (s.c.) at 50 IU/kg bodyweight for 10 consecutive days before completing all behavioral tests. Drug dosage and timing of administration were determined based on previous studies (Kwatra et al, 2020;Jiang et al, 2022). A JNK agonist, anisomycin (AN, MedChemExpress, United States), and a p38 agonist, phorbol 12-myristate 13-acetate (PMA, MedChemExpress, United States) were dissolved in sterile 0.9% saline and injected intraperitoneally (i.p.)…”

Section: Drug Administrationmentioning

confidence: 99%

“…In addition, sCT can take effect by activating CTR or/and AMYRs (Arans et al, 2021). Similarly, our group has recently demonstrated that an acute administration of sCT could ameliorate a depressive-like phenotype by activating AMYRs (Jiang et al, 2022). However, the mechanism of the sCT's antidepressant effect remains to be elucidated.…”

Section: Introductionmentioning

confidence: 96%

See 4 more Smart Citations

Chronic salmon calcitonin exerts an antidepressant effect via modulating the p38 MAPK signaling pathway

Wenhui

Li²,

Jiang³

et al. 2023

Front. Mol. Neurosci.

Self Cite

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Chronic Restraint Stress Modelmentioning

confidence: 99%

Section: Drug Administrationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 96%

See 3 more Smart Citations

Chronic salmon calcitonin exerts an antidepressant effect via modulating the p38 MAPK signaling pathway

Wenhui

Li²,

Jiang³

et al. 2023

Front. Mol. Neurosci.

Self Cite

View full text Add to dashboard Cite

show abstract

Assessing suicide risk in chronic pain management: a narrative review across drug classes

Brezic,

Gligorevic,

Candido

et al. 2024

Expert Opinion on Drug Safety

View full text Add to dashboard Cite

The gut metabolite indole-3-propionic acid activates ERK1 to restore social function and hippocampal inhibitory synaptic transmission in a 16p11.2 microdeletion mouse model

Jiang,

Wang,

Jiang

et al. 2024

Microbiome

Self Cite

View full text Add to dashboard Cite

Background Microdeletion of the human chromosomal region 16p11.2 (16p11.2$${}^{+/-}$$ + / - ) is a prevalent genetic factor associated with autism spectrum disorder (ASD) and other neurodevelopmental disorders. However its pathogenic mechanism remains unclear, and effective treatments for 16p11.2$${}^{+/-}$$ + / - syndrome are lacking. Emerging evidence suggests that the gut microbiota and its metabolites are inextricably linked to host behavior through the gut-brain axis and are therefore implicated in ASD development. Despite this, the functional roles of microbial metabolites in the context of 16p11.2$${}^{+/-}$$ + / - are yet to be elucidated. This study aims to investigate the therapeutic potential of indole-3-propionic acid (IPA), a gut microbiota metabolite, in addressing behavioral and neural deficits associated with 16p11.2$${}^{+/-}$$ + / - , as well as the underlying molecular mechanisms. Results Mice with the 16p11.2$${}^{+/-}$$ + / - showed dysbiosis of the gut microbiota and a significant decrease in IPA levels in feces and blood circulation. Further, these mice exhibited significant social and cognitive memory impairments, along with hyperactivation of hippocampal dentate gyrus neurons and reduced inhibitory synaptic transmission in this region. However, oral administration of IPA effectively mitigated the histological and electrophysiological alterations, thereby ameliorating the social and cognitive deficits of the mice. Remarkably, IPA treatment significantly increased the phosphorylation level of ERK1, a protein encoded by the Mapk3 gene in the 16p11.2 region, without affecting the transcription and translation of the Mapk3 gene. Conclusions Our study reveals that 16p11.2$${}^{+/-}$$ + / - leads to a decline in gut metabolite IPA levels; however, IPA supplementation notably reverses the behavioral and neural phenotypes of 16p11.2$${}^{+/-}$$ + / - mice. These findings provide new insights into the critical role of gut microbial metabolites in ASD pathogenesis and present a promising treatment strategy for social and cognitive memory deficit disorders, such as 16p11.2 microdeletion syndrome.

show abstract

Salmon Calcitonin Exerts an Antidepressant Effect by Activating Amylin Receptors

Cited by 5 publications

References 48 publications

Chronic salmon calcitonin exerts an antidepressant effect via modulating the p38 MAPK signaling pathway

Chronic salmon calcitonin exerts an antidepressant effect via modulating the p38 MAPK signaling pathway

Assessing suicide risk in chronic pain management: a narrative review across drug classes

The gut metabolite indole-3-propionic acid activates ERK1 to restore social function and hippocampal inhibitory synaptic transmission in a 16p11.2 microdeletion mouse model

Contact Info

Product

Resources

About