Abstract
Acute fasting induced antidepressant‐like effects. However, the exact brain region and mechanism of these actions are still largely unknown. Therefore, in this study the antidepressant‐like effects of acute fasting on c‐Fos expression and BDNF levels were investigated. Consistent with our previous findings, immobility time was remarkably shortened by 9 hrs fasting in the forced swimming test. Furthermore, these antidepressant‐like effects of 9 fasting were inhibited by a 5‐HT 2A/2C receptor agonist (±)‐1‐(2, 5‐dimethoxy‐4‐iodophenyl)‐2‐aminopropane hydrochloride (DOI), and the effect of DOI was blocked by pretreatment with a selective 5‐HT 2A receptor antagonist ketanserin. Immunohistochemical study has shown that c‐Fos level was significantly increased by 9 hrs fasting in prefrontal cortex but not hippocampus and habenular. Fasting‐induced c‐Fos expression was further enhanced by DOI in prefrontal cortex, and these enhancements were inhibited by ketanserin. The increased BDNF levels by fasting were markedly inhibited by DOI in frontal cortex and hippocampus, and these effects of DOI on BDNF levels were also blocked by ketanserin. These findings suggest that the antidepressant‐like effects of acute fasting may be exerted via 5‐HT 2A receptor and particularly sensitive to neural activity in the prefrontal cortex. Furthermore, these antidepressant‐like effects are also mediated by CREB and BDNF pathway in hippocampus and frontal cortex. Therefore, fasting may be potentially helpful against depression.
Highlights
Caloric restriction or fasting has been shown to be associated with significantly improvements in brain function [1–4]
The immobility time was remarkably inhibited by 9 hrs fasting but not 18 hrs in the forced swimming test (FST)
We have found that the inhibitory effects of DOI on acute fasting-induced antidepressant effects were reversed by the 5HT2A receptor antagonist ketanserin
Summary
Caloric restriction or fasting has been shown to be associated with significantly improvements in brain function [1–4]. Other and our studies have shown that caloric restriction and fasting may improve depression in rodents [3, 4]. Our study has shown that immobility time in the forced swimming test (FST) was remarkably inhibited by 9 hrs but not 3 and 18 hrs of fasting without change of locomotor activity [4]. The antidepressant-like actions of 9 hrs fasting were inhibited by a 5HT2A/2C receptor agonist (Æ)-1-(2, 5-dimethoxy-4-iodophenyl)-2-aminopropane hydrochloride (DOI). These data reveal that 5-HT2 receptor may be involved in the antidepressant-like effects induced by acute fasting
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