by Summary: When neural assemblies between the hippocampus and the prefrontal cortex are not synchronized at the right time, memories are lost.
Source: University of Bristol
Learning, remembering, and remembering memories is supported by several separate groups of neurons that are connected within and across key regions in the brain. When these neural assemblies don’t synchronize at the right time, memories are lost, a new study led by the Universities of Bristol and Heidelberg has found.
How do you keep track of what to do next? What happens in the brain when the head is empty? Short-term memory relies on two key regions of the brain: the hippocampus and the prefrontal cortex.
The researchers wanted to find out 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 BiologyShe also wanted to understand why memory sometimes fails.
“Neural assemblies” – groups of neurons that combine to process information – were first proposed over 70 years ago, but have proven difficult to localize.
Using brain recordings in rats, the research team showed that memory encoding, storage and retrieval are aided by dynamic interactions involving multiple neural assemblies formed within and between the hippocampus and the prefrontal cortex. When these gatherings fail to coordinate, the animals make mistakes.
dr Michał Kucewicz, Assistant Professor of Neurology at Gdańsk University of Technology, formerly Ph.D. University of Bristol student and lead author, said: “Our results make potential therapeutic interventions for memory restoration more difficult to achieve spatially and temporally.
“On the other hand, our results have identified critical processes that determine success or failure in remembering. These represent viable targets for therapeutic interventions at the level of interactions with neural assemblies.”
Matt Jones, Professor of Neuroscience at the School of Physiology, Pharmacology and Neuroscience and Bristol Neuroscience and senior author of the article, added: “Our results demonstrate that the neural substrates of memory are more distributed in anatomical space and more dynamic over time than previously thought on the basis of neuropsychological models.”
The next steps for research would be to modulate the interactions of neural assemblies, either through 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 hypothesize that the same mechanisms would work in human patients to restore memory functions that are impaired in a specific brain disorder.
About this news from memory and neuroscience research
Author: press office
Source: University of Bristol
Contact: Press Office – University of Bristol
Picture: The image is in the public domain
Original research: Open access.
“Different hippocampal-prefrontal neural assemblies coordinate the encoding, maintenance, and recall of memory” by Aleksander PF Domanski et al. Current Biology
Abstract
Distinct hippocampal-prefrontal neural assemblies coordinate the encoding, maintenance, and recall of memories
highlights
- Hippocampal-cortical (CA1-PFC) activity reconfigures during different memory states
- Distributed CA1-PFC arrays fire together with a 5 Hz rhythm during memory loading
- Tiled activation in PFC preserves memory across delay periods
- The breakdown of rhythmic CA1-PFC arrays heralds unstable delay encoding and errors
Summary
Short-term memory allows for the inclusion of recent experiences in subsequent decision-making. This processing recruits both the prefrontal cortex and the hippocampus, where neurons encode task cues, rules, and outcomes. However, it is still unclear which information is transported when exactly by which neurons.
Using population decoding of activity in the rat medial prefrontal cortex (mPFC) and dorsal hippocampal CA1, we confirm that mPFC populations result in sample information about delays in operant mismatch with sample application being maintained, even though individual neurons fire only transiently .
During sample encoding, different mPFC subpopulations joined distributed CA1 mPFC cell arrays characterized by 4-5 Hz rhythmic modulation; CA1-mPFC accumulations reappeared during election episodes but were not modulated at 4-5 Hz. Delay-dependent errors emerged when attenuated rhythmic montage activity heralded the collapse of sustained mPFC encoding.
Our results map component processes of memory-driven decisions to heterogeneous CA1-mPFC subpopulations and the dynamics of physiologically different, distributed cell assemblies.
