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Depending on the strength of the connection between different nerve centers, the brain may tend to either be dependent on something or depression.

Our sense of pleasure depends on the reward system, or the reinforcement system, which is a complex of nerve centers. The reinforcement system does not just give us a feeling of pleasure, it connects it with this or that action or event, why it is called so — our actions are reinforced by something pleasant in the form of a reward. Therefore, it is clear that the reinforcement system plays a huge role in motivation, in training, in managing attention – all these things are somehow tied to pleasure. Roughly speaking, just as a dog is motivated to give a paw in order to get sugar, so a person is motivated to go to work to get praise and a cash reward.

Although, of course, a person is not so simple. First, our motivations can be quite complex, purely internal, depending on our personal values. Secondly, the reinforcement system does not exist by itself, other nerve centers that control the higher nervous activity constantly interact with it – they set the framework for the reinforcement system, plan its work, or simply limit it in desires. It happens, however, that the neural system of checks and balances fails, and then we are dealing with dependence — on food, on alcohol, on opiates, on purchases, etc. The other extreme is depression with anhedonia, or the inability to experience joy either from what; it is obvious that in this case, a person will completely extinct all motivation for any activity.

Since the nerve centers that make up the reinforcement system work together and must constantly exchange information with each other, it can be assumed that neuropsychiatric problems, such as addictions and depression, are at least partially related to the problems of information transfer between the centers of this system. It is known that dependencies are indeed accompanied by a too strong connection between the hippocampus (the memory center, which is included in the reward system) and the adjacent nucleus (which is often called simply the pleasure center).

Researchers at the University of Maryland decided to directly test how the gain and weakening of the connection between the hippocampus and the adjacent nucleus affect behavior. The neurons that form this connection in mice were modified by optogenetic methods so that they respond to light. With the help of optical fiber implanted in the brain, activated communication channel between the two brain centers; and this communication channel was getting stronger. As a result, as stated in an article in Nature, mice had the memory of a false reward. The animals were motivated to take certain actions, and a day later they returned to the place where they were stimulated by neurons – although they received no real reward. It is worth emphasizing that the researchers acted not on the hippocampus, not on the pleasure center, but on the information “bus” between them.

Then the authors of the work acted differently: in mice, other neurons were modified, which suppress the activity of nerve cells between the hippocampus and the pleasure center. Now, when using neurons-suppressors with the help of light, they weakened this communication channel — and before that, communicative mice stopped coming to where they communicated with their comrades. For social rodents, this behavior is an anomaly that is a sign of depression; because with depression, there really is no motivation to communicate with others.

Moreover, when initially depressed mice were taken for an experiment (and animals can be simulated signs of depression, although this is not a real, “human” depression), it turned out that the connection between the hippocampus memory center and their pleasure center is weak – and what is important, direct stimulation of neurons does not enhance it. However, if the animals were given antidepressants, the information channel returned to normal, and they could create a false memory of pleasant things, as described above.

The depressed brain has other features; For example, last year we wrote that because of certain features in the structure of serotonin neurons during depression, serotonin ceases to flow into the nerve centers. On the other hand, the more we know about the mechanism of depression, the sooner we will find some effective remedy for it. Since the connection between the hippocampus and the nucleus accumbens plays a role both in the formation of dependencies and in depressions, it is possible that both dependencies and depression can be overcome by acting on the neurons connecting these two nerve centers.