Scientists Take Step Toward Mapping How The Brain Stores Memories

Scientists Take Step Toward Mapping How the Brain Stores Memories

A new study led by scientists at The Scripps Research Institute (TSRI) sheds light on how the brain stores memories. The research, published recently in the journal eLife, is the first to demonstrate that the same brain region can both motivate a learned behavior and suppress that same behavior.

“We behave the way we do in a specific situation because we have learned an association—a memory—tying an environmental cue to a behavior,” said Nobuyoshi Suto, TSRI Assistant Professor of Molecular and Cellular Neuroscience, who co-led the study with TSRI Professor Friedbert Weiss and Bruce Hope, a principal investigator at the National Institutes of Health’s National Institute on Drug Abuse. “This study provides causal evidence that one brain region can store different memories.”

Scientists know that our memories are stored in specific areas of the brain, but there has been some debate over whether a single brain region can store different memories that control opposing behavior. For example, can the same region store the meanings of red and green traffic lights—the memories that make a driver stop a car at a red light, then hit the gas pedal at a green light?

Suto’s research focuses specifically on the brain circuits that control motivation. In the new study, he and his colleagues set out to examine how rats learn to press levers to get sugar water—and where they store those motivational memories.

The researchers first trained the rats to press a lever to get sugar water. The researchers then trained the rats to recognize two colored lights: one signaling the availability of sugar reward, and the other signaling the omission of this reward. As a consequence, the animals learned to change their behavior in response to these cues: the cue signaling availability promoted the lever-pressing, while the cues signaling omission suppressed this reward-seeking behavior.

Based on previous electrophysiology studies, Suto and his colleagues speculated that memories associated with these two lessons were both stored in a region of the brain called the infralimbic cortex.

“We’ve seen correlational evidence, where we see brain activity together with a behavior, and we connect the dots to say it must be this brain activity causing this behavior,” said Suto. “But such correlational evidence alone cannot establish the causality—proof that the specific brain activity is directly controlling the specific behavior.”

So scientists took their experiment a step further. Using a pharmacogenetics approach, the researchers selectively switched off specific groups of brain cells—called neural ensembles—that react to select cues signaling either reward availability or reward omission.

The experiments demonstrated that distinct neural ensembles in the same region directly controlled the promotion of reward-seeking or the suppression of that behavior. Without those neurons firing, the rats no longer performed the behavior motivated by the memories in those ensembles. At last, the scientists appeared to prove the causality.

Suto called the findings a step towards understanding how different memories are stored in the brain. He said the research could also be relevant for studying which neurons are activated to motivate—and prevent—drug relapse. He said he’d next like to look at what other regions in the brain these infralimbic cortex neurons may be communicating with. “Brain regions don’t exist in a vacuum,” he said. In addition, he also would like to determine the brain chemicals mediating the promotion or suppression of reward seeking.

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(Image caption: diagram of the research findings (Taken from article’s Table of Contents Image) bFGF is produced in the injured zone of the cerebral cortex. Ror2 expression is induced in some population of the astrocytes that receive the bFGF signal, restarting their proliferation by accelerating the progression of their cell cycle)

How brain tissue recovers after injury: the role of astrocytes

A research team led by Associate Professor Mitsuharu ENDO and Professor Yasuhiro MINAMI (both from the Department of Physiology and Cell Biology, Graduate School of Medicine, Kobe University) has pinpointed the mechanism underlying astrocyte-mediated restoration of brain tissue after an injury. This could lead to new treatments that encourage regeneration by limiting damage to neurons incurred by reduced blood supply or trauma. The findings were published on October 11 in the online version of GLIA.

When the brain is damaged by trauma or ischemia (restriction in blood supply), immune cells such as macrophages and lymphocytes dispose of the damaged neurons with an inflammatory response. However, an excessive inflammatory response can also harm healthy neurons.

Astrocytes are a type of glial cell*, and the most numerous cell within the human cerebral cortex. In addition to their supportive role in providing nutrients to neurons, studies have shown that they have various other functions, including the direct or active regulation of neuronal activities.

It has recently become clear that astrocytes also have an important function in the restoration of injured brain tissue. While astrocytes do not normally proliferate in healthy brains, they start to proliferate and increase their numbers around injured areas and minimize inflammation by surrounding the damaged neurons, other astrocytes, and inflammatory cells that have entered the damaged zone. Until now the mechanism that prompts astrocytes to proliferate in response to injury was unclear.

The research team focused on the fact that the astrocytes which proliferate around injured areas acquire characteristics similar to neural stem cells. The receptor tyrosine kinase Ror2, a cell surface protein, is highly expressed in neural stem cells in the developing brain. Normally the Ror2 gene is “switched off” within adult brains, but these findings showed that when the brain was injured, Ror2 was expressed in a certain population of the astrocytes around the injured area.

Ror2 is an important cell-surface protein that regulates the proliferation of neural stem cells, so the researchers proposed that Ror2 was regulating the proliferation of astrocytes around the injured areas. They tested this using model mice for which the Ror2 gene did not express in astrocytes. In these mice, the number of proliferating astrocytes after injury showed a remarkable decrease, and the density of astrocytes around the injury site was reduced. Using cultured astrocytes, the team analyzed the mechanism for activating the Ror2 gene, and ascertained that basic fibroblast growth factor (bFGF) can “switch on” Ror2 in some astrocytes.

This research showed that in injured brains, the astrocytes that show (high) expression of Ror2 induced by bFGF signal are primarily responsible for starting proliferation. bFGF is produced by different cell types, including neurons and astrocytes in the injury zone that have escaped damage. Among the astrocytes that received these bFGF signals around the injury zone, some express Ror2 and some do not. The fact that proliferating astrocytes after brain injury are reduced during aging raises the possibility that the population of astrocytes that can express Ror2 might decrease during aging, which could cause an increase in senile dementia. Researchers are aiming to clarify the mechanism that creates these different cell populations of astrocytes.

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*Glial cell: a catch-all term for non-neuronal cells that belong to the nervous system. They support neurons in various roles.

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