Individual nerve brain cells activate immune proteins to consolidate certain unpleasant events in memory.
Memory formation is associated with the transformation of networks of nerve cells. Some connections between neurons are strengthened, others are born, and some disappear. Transformations are accompanied by intense changes in the genetic and molecular apparatus. Often, scientists discover one or the other gene or protein substance that is involved in the formation of memory and retains information. However, the entire molecular genetic mechanism of memory support still remains a mystery to us.
In their recent work, scientists described a group of nerve cells located in the hippocampus. The mechanism of operation of these structures has become relatively clear: after special DNA damage, inflammation processes are launched in them.
Representatives of the A. Einstein School of Medicine conducted an experiment on rodents: under certain conditions, a weak current was sent to their paws, activating the method of remembering unpleasant events. Further, if the rodent was reintroduced to the same cage in which it had received the shock, the animal would freeze in alarm, demonstrating a stress response. According to scientists, in certain nerve cells of the hippocampus after exposure to stress, an inflammatory reaction is formed due to communication with the protein agent TLR9 or toll-like receptors.
This type of receptor belongs to the class of innate immune defense: they demonstrate a response to manifestations typical of large pathogenic groups. If there is a threat, these receptors initiate certain processes within the cellular structure and notify neighboring cells and the immune system about the problem.
In ordinary hippocampal nerve cells, memory genes are quickly turned on after DNA damage. The TLR9 protein is needed to store the necessary information in memory: when this protein was turned off, rodents did not remember for a long time an unpleasant situation - in particular, the stress they experienced when exposed to an electric current.
How does TLR9 turn on? DNA appeared in the cytoplasm of nerve cells, placed in special membrane vesicles. Active TLR9 triggered the process of DNA repair: in this case, a whole series of regulatory proteins appeared, and DNA particles were grouped at the cell organelle - the centrosome. Thus, DNA particles indicating genomic damage, together with TLR9 and other protein substances, triggered DNA repair in the cell nucleus. This entire process pursued only one goal - the formation of long-term memory.
Despite the fact that TLR9 is an immune protein associated with the inflammatory response, we are not talking about an inflammatory process in the full sense of the word: nerve cells continue to function and exist normally. In total, two similar mechanisms of immunity and neural memory are used, which have the same molecular set of tools. It is quite possible that at some stages there are still differences. However, scientists will have to study these questions in subsequent studies.
Details on the Nature magazine