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Happiness hormone can cause depression

13.12.2015

The neurotransmitter serotonin is often referred to as the "happiness hormone". Molecules such as serotonin are used to transmit nerve impulses between nerve cells, and it has long been noted that a chronic lack of serotonin can lead to constant anxiety and depression: neurons in the nerve circuits responsible for emotional "positivity" communicate worse due to that they lack their neurotransmitter. Therefore, the action of many antidepressants is calculated on the fact that they will increase the level of serotonin in interneuronal synapses, thereby contributing to a positive emotional mood. (However, there is still a lot of uncertainty about the mechanism of action of antidepressants, and they still surprise neuroscientists - for example, we recently wrote that some of them are able to influence epigenetic modifications in cellular DNA.)

Through emotions, serotonin can influence behavior. For example, a few years ago, researchers from Oxford found that this neurotransmitter affects our perception of other people's relationships: the more it was, the more a person was inclined to evaluate other people's relationships as very romantic and very close (photos of couples were offered as an example for evaluation); and vice versa - with low levels of serotonin, other people's relationships seemed less close. And in 2012, Kyoto University staff published an article in the PNAS journal that talked about the relationship between brain serotonin levels and our sense of justice: the more serotonin, the more dishonesty we are willing to forgive another person.

However, as Mark S. Ansorge and his colleagues at Columbia University show, the results of serotonin are not that simple: its effect depends on where in the brain it is present. It is known that it is synthesized by the nuclei of the suture - the so-called clusters of neurons located along the midline of the medulla oblongata. The raphe nuclei are divided into several groups, among which there is an upper central nucleus and a dorsal nucleus. Both of them produce serotonin, which is used by other brain systems, but the nuclei's own neurons also respond to it, and for a long time it was not clear how the activity of local nerve cells affects behavior.

The experiments were carried out on mice, some of which were normal healthy animals, while others stimulated anxiety and depression. It turned out that the serotonin neurons of the raphe nuclei work differently in both. For example, an increase in anxiety was accompanied by an increase in the activity of the upper central nucleus; on the other hand, depression in mice weakened with a decrease in the activity of the same upper central nucleus, but increased with a decrease in the activity of the dorsal nucleus. The full results of the experiments are published in Cell Reports.

In other words, neurons using serotonin do not necessarily give only joy and happiness. Positive emotions rather depend on the balance of activities of different groups of serotonin neurons: if the balance is strongly skewed in one direction, then depression and anxiety will come instead of joy and happiness, although there may be more than enough serotonin. Of course, after mice, it will be necessary to check whether the serotonin nuclei of the raphe work in humans in this way, and if everything is really so, it is worth thinking about new antidepressants that would not just act on the level of one or another neurotransmitter, but would focus on some particular brain area.

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