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Antidepressants are a lifeline – literally – for millions of people. But for a surprising 30%, they do not work at all. This chasm can be attributed to the prevailing knowledge of depression, based on observation that it tends to flare up when your monoamine (ie, serotonin) neurotransmitters are down. . This discovery is being made for the production of selective serotonin reuptake inhibitors (SSRIs).
But the fact that SSRIs do not work for so many people indicates that there is something else that causes depression. A milestone in Yumiko Saito and Yuki Kobayashi, neuroscientists at the University of Hiroshima, Japan, whose research has contributed significantly to answering this question. "1965" "Thirty percent of people on these drugs (SSRIs) feel no effect". "Saito's previous research had led to the discovery that the RGS8 protein, emitted in the brain, helps control MCHR1 – a hormone receptor involved in appetite, sleep, and emotional responses." In vitro, RGS8 has been shown to inactivate MCHR1, a process that – in theory – alleviates the symptoms of depression.
In order to push the research a little closer to realization (read: human use), the team experimented with two of the mouse: a set with "regular" brain chemistry, and the other chemically designed to display higher levels of RGS8.
In an exploit reminiscent of the seven sports lessons, mice were subjected to a forced swimming test: Those who telephoned in their swimming efforts were counted as having the most depressive characteristics, their immobility badimilated to "giving up".
READ MORE: your you genetically at risk for depression
The results were illuminating; Mice fed RGS8 showed shorter periods of immobility, indicating more swimming time, and therefore lower levels of depression. During treatment with the antidepressant desipramine, which acts on monoamines, the immobilization times of the mice were further curbed.
Meanwhile, "regular" mice received the drug SNAP94846, which prevents the operation of MCHR1. This significantly reduces their immobility time, while the same drug administered to RGS8-impregnated mice has no effect on their depression. As such, the experiment seems to reveal a "new type of depression," says Saito, in which monoamines are not involved in depressive behavior, but rather MCHR1.
After further investigation, RGS8-boosted neuronal lice-boosted mice (the place where MCHR1 is located) than their counterfeited counterparts. The team still does not know exactly what causes this link, but they do not think it's an accident: "[I] we can badume that a significant change in eyelash length can to be badociated with the behavioral consequences observed in RGS8 [mice]] Explains the report
If RGS8 actually plays a "modulating role […] in the neurobiology of depressive behavior", future modulations of its levels and functions could provide a viable and revolutionary treatment for depression and other mood disorders – that's where you are: if you have exhausted your healthy diet, regular exercise, and meditation thoughts, and your mood is still infinitely low, your respective levels of RGS8 and MCHR1 may be the same.There is a long way to go before the treatment is tested on humans – treatments that on mice often fail mankind – but it certainly provides preliminary insight into a disease that confuses both psychiatrists and patients
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