Scientists in Japan have discovered they can temporarily erase fear memories by blocking specific neurotransmitter cells with specially designed light sensitive antibodies, a technique that may have application in psychiatric treatment.
The team of researchers from Yokohama City University, Osaka University and the University of Tokyo explained in their study published in Nature Biotechnology that their technique was more precise than earlier methods of blocking neurotransmitters—the chemical messengers that carry information between nerve cells —because it targeted only the surface of the cells where the neurotransmitters function, and not the cells’ internal proteins, thus avoiding long-lasting damage.
The scientists used a method called chromophore-assisted light inactivation (CALI), a technique that has previously been used to investigate the function of proteins. The process “uses light irradiation to generate a temporary toxic form of oxygen that causes an area of damage shorter than a typical protein-protein interaction distance,” the study explained, which allowed the researchers to precisely target a specific neurotransmitter receptor called GluA1 in the brains of mice.
The researchers created an antibody containing a light-sensitive molecule against the protein on the outer surface of the GluA1 neurotransmitter, and injected it into the hippocampus, a part of the brain involved in memory and navigation, the study explained.
Having identified GluA1 as the neurotransmitter that carried fear information in an earlier experiment using rats, the research team created an experiment in which mice were allowed to move between light and dark boxes, but received a mild electric shock in the dark boxes so they would favor the light ones.
However, “In response to illumination of the mouse hippocampus with green light, we found that mice returned to the dark boxes more quickly than control animals,” said study first author Kiwamu Takemoto, an assistant professor at Yokohama City University. “This showed that the fear memory had been erased by the inactivation of synaptic GluA1.”
The scientists noted that the effect was short-lived, less than 24 hours, because the mouse brains replaced the ‘tainted’ GluA1 neurotransmitter with a similar protein GluA2, after which the mice retained their fear memory and avoided the dark boxes.
Although the scientists noted the work was very preliminary, they suggested that if developed further the technique could have applications in psychiatric therapy and other mental health treatments.