The study was published in the NeuroImage Journal.
Bradley LegaMD, an associate professor of neurological surgery, neurology and psychiatry, said his findings may point to new deep stimulation treatments for other brain diseases and injuries.
“It sheds light on an important question, how do you know you remember something from the past compared to experiencing something new that you’re trying to remember?” said Dr. Lega, a member of the Peter O’Donnell Jr. Brain Institute.
The most significant finding was that the firing occurred at a different timing compared to other brain activity when memories were retrieved. This small difference in timing, called “phase deviation,” had not been reported in humans before. Together, these results explained how the brain can “re-experience” an event, but also track whether memory is something new or something previously encoded.
“This is one of the clearest evidence to date to show us how the human brain works in remembering old memories compared to forming new ones,” Dr. Lega said.
His study identified 103 memory-sensitive neurons in the hippocampus and entorhinal cortex of the brain that increased their activity when memory encoding was successful. The same pattern of action returned when patients tried to remember these same memories, especially highly detailed memories.
This cerebral edema may play a role in schizophrenia because hippocampal dysfunction is underlying the inability of schizophrenics to interpret memories and hallucinations or delusions.
“The neurons identified by Dr. Legan are an important part of the puzzle as to why this happens,” he said Carol Tamminga, MD, Professor and Director of Psychiatry and National Expert in Schizophrenia.
“Hallucinations and delusions in people with psychotic illness are real memories that are processed through nervous memory systems, such as ‘normal’ memories, even if they are corrupted. It would be important to understand how this ‘phase deviation mechanism’ can be used to modify these impaired memories,” Dr. Tamminga added.
The opportunity to learn more about human memory arose from surgeries in which electrodes implanted in the brains of epileptic patients to map patient seizures could also be used to identify neurons involved in memory. In this study, 27 epileptic patients who were implanted with electrodes at UT Southwestern and Pennsylvania Hospital participated in memory tasks to provide information for the brain study.
The analysis of the data does not conclusively prove it, but added new credibility to an important memory model called Separate Phases at Encoding and Retrieval (SPEAR), which the researchers developed from rodent studies.
“It’s never been nailed. It’s one thing to get a model; it’s another thing to show evidence that this happens to humans,” Dr. Lega said.
The SPEAR model, which predicted the “phase deviation” reported in the study, was developed to explain how the brain can track new versus old experiences in memory retrieval. Previously, the only evidence to support SPEAR came from rodent models.
This study was supported by National Institutes of Health grants R01NS125250 and R01NS106611.
Dr. Tamminga works in the Stanton Sharp Distinguished Chair in psychiatry.
Source: ANI