Cheer for your health
Taking the signal "I'm sick", the brain changes our behavior
When we are sick, we do not want to eat, drink and walk: our only desire is to curl up under a blanket. Most animals behave in a similar way with infections. Now scientists have found out how the brain coordinates this almost universal and quite adaptive "painful behavior".
During millions of years of evolution, all creatures, from bacteria and viruses to mammals, participated in a kind of "arms race". In order to survive and win the competition, we had to attack and defend ourselves. And all living organisms have developed various survival strategies that provide an advantage in this struggle, or the opportunity to evade it altogether.
One of the adaptive reactions of mammals in response to infections of different nature is a change in physiological and behavioral reactions, including an unwillingness to eat, drink and move. And this is not the result of the direct action of an infectious agent (at least, not always), but part of the generalized response of the body to the pathogen. This is proved by experiments on animals in which forced feeding with bacterial infection increased mortality.
To understand which parts of the brain are responsible for behavioral changes in the disease, a group of scientists from the United States and China conducted experiments on laboratory mice that were injected with lipopolysaccharide, a component of the bacterial cell wall that activates the immune system and causes painful manifestations. This procedure is typically used to simulate an infectious lesion in a laboratory.
Already 1-3 hours after the injection of bacterial polysaccharide, scientists observed a surge of activity in one of the brain stem regions (more specifically, in the dorsal vagus nerve complex), and then identified a population of neurons producing the neuropeptide ADCYAP1, which were responsible for this activation.
To prove the role of these nerve cells in the formation of "painful behavior", the researchers activated them in healthy mice and deactivated them in those who received lipopolysaccharide. The former began to behave like patients, while the latter did not change their behavior in response to the provoking injection.
How is everything going? Lipopolysaccharide activates the immune system, stimulating its cells to produce pro-inflammatory cytokine molecules that cause painful manifestations. Afferent ("bringing") neurons of the vagus nerve are located in the area of the brain reacting to infectious agents, which play an important role in transmitting its signals to higher nerve centers. For example, this area transmits information to the brain that something harmful has been eaten, and as a result, the desire to eat this food disappears. These neurons also carry receptors for proinflammatory cytokines, providing transmission to the brain of signals leading to the same loss of appetite.
Of course, the mechanism linking the immune response to the neural pathways regulating adaptive "painful behavior" is described so far only in general terms. But now it has become more clear what the brain is "busy" with when our body is fighting infection.
Article by Ilanges et al. Brainstem ADCYAP1+ neurons control multiple aspects of sickness behavior is published in the journal Nature.
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