Involvement of nitric oxide pathway in the acute anticonvulsant effect of salmon calcitonin in rats

Filiz, Ahmet Kemal; Karabulut, Sebahattin

doi:10.1016/j.eplepsyres.2022.106864

Cited by 2 publications

(1 citation statement)

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“…Taskiran and Filiz showed that sCT had antiepileptic activity in Pentylenetetrazole (PTZ)-induced epileptic seizures in rats through excitatory-inhibitory, oxidative stress and neuroinflammation pathways. After PTZ induced epileptic seizures, sCT even displayed neuroprotective effects on hippocampal neurons (Taskiran et al, 2020;Filiz and Karabulut, 2022). Moreover, sCT can regulate the alcohol intake of mice by activating the mesolimbic dopamine system (Kalafateli et al, 2021).…”

Section: Discussionmentioning

confidence: 99%

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

Wenhui

Li²,

Jiang³

et al. 2023

Front. Mol. Neurosci.

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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.

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Section: Discussionmentioning

confidence: 99%