For much of the history of brain science, the word “engram” has been a bit of a catch-all term, referring to the hypothetical physical incarnation of memory. If this turned out to be a storm of electrical activity, then that’s what the engram would be; if it turned out that networks of physical neurons were the home of specific memories, then an engram was that, instead.
Lately, though, the word has gotten a lot more specific. We now have the term “memory neurons” to refer to the nerve cells of the hippocampus, which seem to play a crucial role in storing and retrieving memories. Since the original proof that at least some memory is localized to specific physical neurons just a few short years ago, understanding of the physical basis of memory has advanced at a lightning pace.
Even in the past year, scientists have made incredible strides. One amazing study may have found the molecular basis for memory formation — the seemingly harmful breakage of DNA. It turns out an enzyme from the topoisomerase family responds to new stimuli by breaking DNA, which seems to activate the transcription of as many as a dozen quick-acting genes associated with neural development. These genes are inhibited by a system of enzymes, but as the now-broken DNA folds up in response to its new situation, these inhibitory genes are blocked, and the now-uninhibited memory genes are free to go out and direct the development of the brain.
Though double-stranded breaks in DNA are generally thought of as being bad for the cell, topoisomerases serve an important role in the cell, breaking, unwinding, and reconnecting the double helix if it’s about to become over-wound and tie itself up into knots. Here, the large-scale conformational change associated with breaking a molecule of DNA acts as a wide-reaching promoter of transcription. By breaking a strand of DNA, a seemingly dangerous thing to do, it can quickly and efficiently activate a wide and physically scattered collection of genes. As we age, our ability to repair such damage to DNA gets less and less powerful — which could help account for the worsened ability to create new short- and long-term memories.
Speaking of long-term memories, a separate study found that the retrieval of long-term memories could one-day be assisted with technology. They showed that by blocking protein synthesis in brain cells, we can stop a mouse from remembering things that it learns — teach it the location of some food while its brain is incapable of strengthening the synaptic pathways between neurons. The mouse will reliably not remember the fact it “learned” just a few hours before but, intriguingly, the researchers could retrieve the memory by artificially causing the specific learning cells associated with the memory to fire.
The researchers say this experimental setup can help to distinguish between the methods of memory formation and memory retrieval. By stopping the mouse brain from strengthening the synaptic connections in response to new info, they seem to have made memory retrieval more difficult. However, when they cause that retrieval to happen on their own, the pattern of synaptic connections associated with that memory will still function properly. This has been interpreted as some of the first evidence showing that augmentation of synapses in these cells of the hippocampus is strongly related to memory.
Study author Tomas Ryan said, “The strengthening of engram synapses is crucial for the brain’s ability to access or retrieve those specific memories, while the connectivity pathways between engram cells allows the encoding and storage of the memory information itself.” These are much more definitive, strident statements than any scientists could have made just five years ago, or even less.
However, it’s almost certainly not that simple. This Stanford team has put forth the idea of mobile memories, in which the hippocampus does indeed store the specifics of new memories in its synaptic connections, but after a while those memories move to elsewhere in the brain. The team found that if they disrupted the hippocampus within a month or so of a new memory, the memory disappeared forever. If they disrupted it after a longer period of time, the memory seemed undisturbed — as though it no longer physically resides in those same cells.
This seems to provide a fairly stark physiological difference that could form the basis for some of the distinctions between short and long term memory — but if the study of memory has taught us anything, it’s that we can’t assume it works in a simple or reasonable way. Occam’s Razor may still apply to the physiology of memory, but when creating such a nuanced aspect of cognition as memory, perhaps it just isn’t possible to slice all that much complexity away.
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