Resume: If the neural connections between the hippocampus and prefrontal cortex don’t synchronize with each other at the right time, memories are lost.
Source: University of Bristol
Learning, remembering, and retrieving memories are supported by multiple distinct groups of neurons connected within and between key brain regions. If these neural assemblies don’t synchronize with each other at the right time, the memories are lost, according to a new study led by the Universities of Bristol and Heidelberg.
How do you keep track of what to do next? What happens in the brain when your mind goes blank? Short-term memory relies on two major brain regions: the hippocampus and the prefrontal cortex.
The researchers sought to determine how these brain regions interact as memories are formed, maintained and recalled at the level of specific groups of neurons.
The study, published in Current Biologyalso wanted to understand why memory sometimes fails.
“Neural assemblies” — groups of neurons that join forces to process information — were first proposed more than 70 years ago, but have proven difficult to pinpoint.
Using brain recordings in rats, the research team has shown that memory encoding, storage and recall is aided by dynamic interactions with multiple neural assemblies formed in and between the hippocampus and prefrontal cortex. When the coordination of these assemblies fails, the animals have made mistakes.
Dr. Michał Kucewicz, assistant professor of neurology at Gdansk University of Technology, formerly a Ph.D. student at the University of Bristol, and lead author, said: “Our results make potential therapeutic interventions for memory recovery more challenging to target across space and time.
“On the other hand, our findings have identified critical processes that determine the success or failure of remembering. These present viable targets for therapeutic interventions at the level of neural assembly interactions.”
Matt Jones, professor of neuroscience in the School of Physiology, Pharmacology and Neuroscience and Bristol Neuroscience and senior author of the paper, added: “Our findings add to the evidence that the neural substrates of memory are more widespread in anatomical space and be more dynamic over time than previously thought on the basis of the neuropsychological models.”
The next steps for the research would be to modulate neural assembly interactions, either using drugs or through brain stimulation, which Dr. Kucewicz is currently doing in human patients, to test whether disrupting or enhancing it would impair or improve memory. The research team hypothesizes that the same mechanisms would work in human patients to restore memory functions compromised by a particular brain disorder.
About this news about memory and neuroscience research
Author: Press Office
Source: University of Bristol
Contact: Press Service – University of Bristol
Image: The image is in the public domain
Original research: Open access.
“Separate hippocampal-prefrontal neural assemblies coordinate memory encoding, maintenance and recall” by Aleksander PF Domanski et al. Current Biology
Different hippocampal-prefrontal neural assemblies coordinate memory encoding, maintenance, and recall
- Hippocampal cortical (CA1-PFC) activity reconfigures during different memory stages
- Co-fire distributed CA1-PFC assemblies with 5 Hz rhythms during memory loading
- Tiled activation in PFC preserves memory during delay periods
- Collapse of rhythmic CA1-PFC assemblies heralds unstable delay encoding and errors
Short-term memory makes it possible to incorporate recent experiences into later decision-making. This processing recruits both the prefrontal cortex and the hippocampus, where neurons encode task cues, rules, and outcomes. However, it remains unclear exactly what information is transmitted when and by which neurons.
Using population decoding of activity in the rat medial prefrontal cortex (mPFC) and dorsal hippocampus CA1, we confirm that mPFC populations lead to retention of sample information about delays of an operant sample mismatch task, despite individual neurons being only transiently firing.
During sample encoding, distinct mPFC subpopulations joined distributed CA1-mPFC cell assemblies characterized by 4–5 Hz rhythmic modulation; CA1-mPFC assemblies re-emerged during choice episodes, but were not modulated at 4–5 Hz. Delay-dependent errors occurred as weakened rhythmic assembly activity heralded the collapse of persistent mPFC encoding.
Our results map component processes of memory-driven decisions to heterogeneous CA1-mPFC subpopulations and the dynamics of physiologically distinct, distributed cell assemblies.