Breakthrough in Memory Research
Jim Windell
Why are some events etched in our memory while others fade into obscurity?
Why will our personal memories of the COVID-19 pandemic likely be etched in our minds with precision and clarity and other things that happened to us in 2020 be forgotten altogether?
The process that mediates why some memories remain strong and others fade away has eluded scientists for many decades, but new research led by the University of Bristol has made a breakthrough in understanding how some memories can be so distinct and long-lasting without getting muddled up with other memories.
The study, entitled “Interneuron-specific Plasticity at Parvalbumin and Somatostatin Inhibitory Synapses onto CA1 Pyramidal Neurons Shapes Hippocampal Output,” and published in Nature Communications, describes a newly discovered mechanism of learning in the brain. This learning stabilizes memories and reduce interference between them. The findings of this research provide new insight into how humans form expectations and make accurate predictions about what could happen in future.
Memories are created when the connections between the nerve cells which send and receive signals from the brain are made stronger. This process has long been associated with changes to connections that excite neighboring nerve cells in the hippocampus, a region of the brain crucial for memory formation.
These excitatory connections must be balanced with inhibitory connections, which dampen nerve cell activity, for healthy brain function. The role of changes to inhibitory connection strength had not previously been considered, and the researchers at the University of Bristol found that inhibitory connections between nerve cells, known as neurons, can similarly be strengthened.
The researchers at the University of Bristol worked in collaboration with computational neuroscientists at Imperial College London and their joint efforts showed how strengthened inhibitory connections allows for the stabilization of memory representations.
These findings uncover for the first time how two different types of inhibitory connections (from parvalbumin and somatostatin expressing neurons) can also vary and increase their strength, just like excitatory connections. Moreover, computational modelling demonstrated this inhibitory learning enables the hippocampus to stabilize changes to excitatory connection strength, which prevents interfering information from disrupting memories.
Lead author Dr. Matt Udakis, Research Associate at the School of Physiology, Pharmacology and Neuroscience, said: "We were all really excited when we discovered these two types of inhibitory neurons could alter their connections and partake in learning. It provides an explanation for what we all know to be true; that memories do not disappear as soon as we encounter a new experience.”
Udakis added that these new findings will help us understand why some memories do not disappear. He also said that the computer modelling gave them important new insight into how inhibitory learning enables memories to be stable over time and not be susceptible to interference. “That's really important as it has previously been unclear how separate memories can remain precise and robust," Udakis said.
Senior author Professor Jack Mellor, Professor in Neuroscience at the Centre for Synaptic Plasticity, said: "Memories form the basis of our expectations about future events and enable us to make more accurate predictions. What the brain is constantly doing is matching our expectations to reality, finding out where mismatches occur, and using this information to determine what we need to learn.
Mellor also stated that they believe that they have discovered new information about how memory plays a crucial role in assessing how accurate our predictions are. “In the current climate, our ability to manage our expectations and make accurate predictions has never been more important," Mellor said.
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Matt Udakis, Victor Pedrosa, Sophie E. L. Chamberlain, Claudia Clopath, Jack R. Mellor. Interneuron-specific plasticity at parvalbumin and somatostatin inhibitory synapses onto CA1 pyramidal neurons shapes hippocampal output. Nature Communications, 2020; 11 (1) DOI: 10.1038/s41467-020-18074-8