Researchers at UT Southwestern Medical Center have identified-characteristics of more than 100 memory-sensitive neurons that play a central role in how memories are recalled in the brain.
The study was published in the “NeuroImage Journal“. Bradley Lega, M.D., associate professor of neurosurgery, neurology and psychiatry, said his findings may point to new deep brain stimulation therapies for other brain diseases and injuries.
“This sheds an important light on the question, how do you know that you are remembering something from the past versus something new that you are trying to remember? Said Dr Lega, fellow of the Peter O’Donnell Jr. Brain Institute.
The most important finding was that the activation occurred at different times than other brain activity when memories were retrieved. This slight difference in timing, called “phase shift”, had not been previously reported in humans.
Together, these findings explained how the brain can ‘relive’ an event, as well as whether the memory is something new or something previously encoded.
“This is one of the clearest evidences to date showing us how the human brain works in terms of old memories memory compared to the formation of new memories,” Dr. Lega said.
His study identified 103 memory neurons in the hippocampal brain and the entorhinal cortex that increased their activity rate when the memory encoding succeeds.
The same scheme of activity came back when patients tried to remember these same memories, particularly detailed memories.
This activity in the hippocampus may be relevant to schizophrenia because the hippocampal dysfunction is the basis of schizophrenic inability to decipher between memories and hallucinations or delusions.
“The neurons identified by Dr. Lega are an important piece of the puzzle as to why this happens,” said Carol Tamminga, M.D., professor and chair of psychiatry and national schizophrenia expert.
“Hallucinations and delusions in people with psychotic illness are real memories, treated by neural memory systems as ‘normal’ memories, even if they are corrupted. It would be important to understand how to use this “phase offset” mechanism to modify these memories. Dr Tamminga added.
An opportunity to learn more about human memory arose from surgeries in which electrodes that were implanted in the brains of patients with epilepsy to map the patients’ seizures could also be used to identify neurons involved in memory.
In this study, 27 patients with epilepsy who were implanted with electrodes at UT Southwestern and a hospital in Pennsylvania participated in memory tasks to generate data for brain research.
Analysis of the data was inconclusive, but it added new credibility to an important memory model called Separate Phases on Encoding and Retrieving (SPEAR) that scientists have developed from studies on rodents.
“It’s never been nailed down. It’s one thing to have a model; another thing is to show proof that this is happening in humans,” said Dr Lega.
The SPEAR model, which predicted the “phase offset” reported in the study, was developed to explain how the brain can follow new experiences compared to those old when engaged in memory retrieval. Previously, the only evidence supporting SPEAR had come from rodent models.
This study was supported by National Institutes of Health grants R01NS125250 and R01NS106611. Dr Tamminga holds the Stanton Sharp Distinguished Chair in Psychiatry.
