Regulating Neural Networks to Preserve Memory

Memory, our ability to record, to preserve and to recall our past experiences, makes up one of the most fundamental and fascinating abilities of our brain. For over forty years, neuroscientists have been interested in the biological mechanisms underlying the storage of the information that our brain records every day. A team from the Faculty of Medicine of the University of Geneva (UNIGE) has demonstrated how the brain regulates the size of the neuronal ensembles that reflect the memory trace to optimize performance. By targeting neurons in the hippocampus, the scientists show that it is possible to inhibit or, on the contrary, to resurface a memory. The study is published in Neuron.

The trace that a memory leaves in our brain is made up by a set of cells located in the hippocampus, called engram. During the encoding of memories, the neurons that form the engram create a network. For a memory to be fixed, the correct number of neurons must be activated. If too many cells are mobilized, the storage of information may become compromised.

To understand how memory works, the Geneva researchers investigated the mechanisms that control the recruitment of neurons into the engram. Initiated by Dominique Muller, who tragically passed away last April, the study was conducted by Pablo Mendez and Christian Lüscher from the Department of Basic Neurosciences at UNIGE Faculty of Medicine.

To weaken or strengthen a memory

To study the long-term stability of memory, the scientists presented mice with a particular situation in order to create a memory. They then exposed these rodents several times to the same situation. By using optogenetics, the researchers stimulated particular neurons. They were thus able to observe that the cells recruited to the engram activate inhibitory cells, which prevent the activation of neighboring neurons. By identifying this inhibition mechanism, the team deciphered how the mobilized neurons control the size of the cell engram and the stability of contextual memory.

Image of hippocampal neurons.
Hippocampal neurons are expressing a protein (in red) that allows one to control neuronal activity with a beam of light. The researchers thus direct the activation of neurons (in green, image on the right). Credit: Pablo Mendez – UNIGE.

Researcher, Pablo Mendez explains “Since we wanted to know to what extent the size of the cell engram influences memory, we used optogenetics to ‘force’ mice to recruit more or less neurons. Subsequently, we found that the more the engram is significant, the better the memory is preserved, but only up to a limited point. Beyond a certain size, memory no longer works. We were thus able to reinforce a memory, but also to remove it.”

“Now that we know the basic mechanism, we want to decipher how memory itself functions. Which cells for which memories? How do neurons really encode memory? We still have many discoveries to make in order to understand in detail how our brain preserves our memories,” explained Christian Lüscher.

About this memory research

Source: UNIGE
Image Source: The image is credited to Pablo Mendez – UNIGE.
Original Research: Abstract for “Hippocampal Somatostatin Interneurons Control the Size of Neuronal Memory Ensembles” by Thomas Stefanelli, Cristina Bertollini, Christian Lüscher, Dominique Muller, and Pablo Mendez in Neuron. Published online February 11 2016 doi:10.1016/j.neuron.2016.01.024


Abstract

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Highlights

•Active neuronal populations inhibit non active neurons during memory formation
•Optogenetic activation of GCs creates an artificial memory and abolishes natural recall
•Non active neurons are excluded from the memory trace via lateral inhibition
•Excitatory neurons activate SST+ interneurons and engage dendritic lateral inhibition

Summary
Hippocampal neurons activated during encoding drive the recall of contextual fear memory. Little is known about how such ensembles emerge during acquisition and eventually form the cellular engram. Manipulating the activity of granule cells (GCs) of the dentate gyrus (DG), we reveal a mechanism of lateral inhibition that modulates the size of the cellular engram. GCs engage somatostatin-positive interneurons that inhibit the dendrites of surrounding GCs. Our findings reveal a microcircuit within the DG that controls the size of the cellular engram and the stability of contextual fear memory.

“Hippocampal Somatostatin Interneurons Control the Size of Neuronal Memory Ensembles” by Thomas Stefanelli, Cristina Bertollini, Christian Lüscher, Dominique Muller, and Pablo Mendez in Neuron. Published online February 11 2016 doi:10.1016/j.neuron.2016.01.02

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