Summary: If neural assemblies between the hippocampus and prefrontal cortex fail to synchronize at the right time, memories are lost.
Source: University of Bristol
Learning, remembering something, and recalling memories are supported by several distinct groups of neurons connected within and across key regions of the brain. If these neural assemblies fail to synchronize at the right time, memories are lost, according to a new study from 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 key brain regions: the hippocampus and the prefrontal cortex.
Researchers have attempted to establish how these brain regions interact with each other when 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 identify.
Using brain recordings in rats, the research team showed that memory encoding, storage and recall are supported by dynamic interactions incorporating multiple neural assemblies formed in and between the hippocampus and cortex. prefrontal. When the coordination of these assemblies fails, animals make mistakes.
Dr Michał Kucewicz, Assistant Professor of Neurology at Gdansk University of Technology, formerly a Ph.D. University of Bristol student and lead author, said: “Our findings make potential therapeutic interventions for memory restoration more difficult to target in space and time.
“On the other hand, our findings have identified critical processes that determine the success or failure of recall. 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 lead author of the paper, added: “Our findings add to the evidence that neural substrates of memory are more distributed in anatomical space and dynamically in time than previously thought based on neuropsychological models.
The next steps in research would be to modulate neural assembly interactions, either using drugs or brain stimulation, which Dr. Kucewicz is currently doing in human patients, to test whether disrupting or increasing them would alter or improve memory. The research team speculates that the same mechanisms would work in human patients to restore impaired memory functions in a particular brain disorder.
About this memory and neuroscience research news
Author: Press office
Source: University of Bristol
Contact: Press Office – University of Bristol
Picture: Image is in public domain
Original research: Free access.
“Distinct hippocampal-prefrontal neural assemblies coordinate memory encoding, maintenance, and recall” by Aleksander PF Domanski et al. Current biology
Distinct Hippocampal-Prefrontal Neural Assemblies Coordinate Memory Encoding, Maintenance, and Recall
- Hippocampal-cortical (CA1-PFC) activity reconfigures during different stages of memory
- Distributed CA1-PFC assemblies trigger with 5 Hz rhythmicity during memory load
- Tiling activation in PFC maintains memory during delay periods
- Collapse of rhythmic CA1-PFC assemblies heralds unstable delay coding and errors
Short-term memory allows recent experience to be incorporated into later decision-making. This processing recruits both the prefrontal cortex and the hippocampus, where neurons encode signals, rules, and task outcomes. However, precisely what information is transported, when and by which neurons remains unclear.
Using population activity decoding in the rat medial prefrontal cortex (mPFC) and dorsal hippocampus CA1, we confirm that mPFC populations lead to maintenance of sample information in time lags. an operative mismatch to the sample task, despite the fact that individual neurons fire only transiently.
During sample encoding, distinct mPFC subpopulations joined distributed CA1-mPFC cell assemblies marked by 4-5 Hz rhythmic modulation; CA1-mPFC assemblies reappeared during choice episodes but were not modulated from 4 to 5 Hz. Delay-dependent errors occurred when attenuated rhythmic assembly activity heralded the collapse of sustained mPFC coding .
Our results map the component processes of memory-guided decisions on heterogeneous CA1-mPFC subpopulations and the dynamics of physiologically distinct distributed cell assemblies.