The lifetime of memories
"Without memory, there is no culture. Without memory, there would be no civilization, no society, no future." Elie Wiesel
Memory is essential for animal survival and gives human beings the extraordinary ability to develop consciousness and ultimately the self. The brain mechanisms that allow us to store, elaborate and recall information from the outside world have been continuously enriched and refined throughout animal evolution. From classical greek philosophers to contemporary neuroscientists, memory has attracted attention because of its profound implications in all aspects of our life. How our lives would be if we could remember every little detail of them? Why do we forget people, places, things and events? Even if answering these questions still needs extensive research, scientists all over the world are continuously and restlessly adding pieces to the long standing scientific question of how memory functions and why it fails in pathological conditions.
Most of our knowledge about human memory arises from clinical studies reporting memory deficits due to brain injuries or developmental and degenerative diseases. A brain surgery aimed to relieve Henry Molaison (1926-2008) from epilepsy, left him unable to form new memories. Congenital abnormalities in the brain of Kim Peek (1951-2009) conferred him an extraordinary memory. These two examples uncover an important fact: brain is able to precisely determine how long particular events of our life will be stored and thus available for recall. But, how does the brain determine the lifetime of memories?
During the formation of memories that we can consciously recall, a small population of neurons in a brain area called dentate gyrus of the hippocampus becomes active. This population is different for each event of our life and, with time, becomes essential to recall that particular memory: when these neurons are silent we are unable to remember but their activation will prompt the recall of that particular experience. This group of neurons is part of the engram (read also the Break: Where is the Engram?), the physical trace of memory in the brain. Modern techniques allow us to identify and count the neurons involved in the encoding of a particular experience. Moreover, using a technique that combines light and genes, called optogenetics, we can activate neurons with light to interfere or recreate their activity during memory formation and recall. In the first part of our study, we used this fascinating technique to artificially add or subtract neurons to the memory engram. The results of these experiments showed that adding neurons to the engram lengthens memory duration while removing neurons decreases memory persistence.
What is then the mechanism that the brain uses to determine the number of neurons in the engram and thus to determine the persistence of a particular memory? In our experiments we observed that engram neurons control the activity of a different type of neurons, named Somatostatin (SST) neurons. Unlike engram neurons that excite target cells, SST neurons are inhibitory cells, and thus silence the neurons they contact. Engram neurons use SST neurons to silence the activity of neighboring neurons in the dentate gyrus, preventing their integration in the memory trace and in this way limiting the persistence of memories.
In our study, we have demonstrated that memories encoded by small number of neurons will be remembered only for a short period of time while a large number of neurons will give raise to memories that will persist longer. SST inhibitory neurons are part of the system that our brain uses to control the size of the engram and thus the lifetime of memories. Defining the mechanisms that limits memory stability bring us closer to understand where are the boundaries of the storage capacity of our brain. Brain pathologies may lead to memory deficits such as in Alzheimer disease but also to "excessive" memories (frequently with associated with bad experiences) such in Posttraumatic stress disorder (read also the Break: Attempts to Forget the Past Make It Harder to Remember the Present). It would be relevant thus to study whether memory storage mechanisms that we describe in our work are compromised in these mental diseases.
Stefanelli T, Bertollini C, Lüscher C, Muller D, Mendez P. Hippocampal Somatostatin Interneurons Control the Size of Neuronal Memory Ensembles. Neuron. 2016;89(5):1074-1085. doi:10.1016/j.neuron.2016.01.024.
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