Originally published on HVMN by Dr. Manuel Lam
The mechanism of acute fasting-induced antidepressant-like effects in mice.
To discover the outcomes in rodents, researchers put mice in an inescapable water tank where they had to swim for 6 minutes. This initiates “social hopelessness”, in which the creature loses would like to get away from the unpleasant circumstance. The departure related “versatility conduct” is then estimated. This is known as the “constrained swim test”, a prominently utilized assessment for stimulant medications.
This mice research showed that 9 hours of fasting essentially repressed “fixed status” in the mice, which was practically identical to an energizer medication called imipramine. This upper impact of intense fasting was obstructed by a serotonin receptor agonist, and thusly, turned around by a serotonin receptor rival called ketanserin.
The expression of two biomarkers was also measured:
C-Fos: A marker of neuronal activation
BDNF: Brain-derived neurotrophic factor, which helps stimulate the process of neurogenesis.
Contrasted with controls, intense fasting upgraded articulation of both of these markers, specifically in the prefrontal cortex for c-Fos and in the frontal cortex and hippocampus for BDNF. Once more, these upgrades were repressed by a serotonin receptor agonist and turned around by ketanserin.
These discoveries propose that fasting might be possibly useful against sadness and that the energizer like impacts of intense fasting might be interceded by means of 5-HT2A receptors, c-Fos, and BDNF pathways.