神经信使受体 z-bo 2020-11-16 361

　　The transmission of chemical messenger (neurotransmitter) receptors at the junction of nerve cells (synapses) is essential for cognitive processes such as memory. By observing the phenomenon after these receptors are inactivated, the corresponding receptor function can be understood. However, if the deactivation is accurate to the location and time then this is only superficial information. Many technologies affect the cell surface and the internal structure of proteins by preventing the action of receptors, while neurotransmitter receptors usually only act on the cell surface. Some Japanese universities, such as Yokohama City University, Osaka University, and Tokyo University, have jointly improved a light-induced method that combines an antibody to generate a large amount of destructive oxygen (CALI: Chromophore Assisted Inactivation) to be specific To inactivate the protein.

　　This technology called CALI has been used in the study of protein function. It uses light radiation to produce a temporary stream of toxic oxygen, which can cause damage to a certain area, and its damage range is shorter than the classical protein-protein interaction. In the current experiment, the researchers obtained an antibody outside of the neurotransmitter receptor GluA1 and labeled it with a photosensitive molecule (photosensitizer). This antibody can specifically inactivate the synaptic response of the GluA1 receptor in cells in vitro and in mice.

　　The team then injected the labeled antibody into the hippocampus of the mouse's brain that controls memory and direction. They then used a fear learning task to evaluate its effect on memory formation: mice shuttled between light and dark boxes and received a foot shock in the dark box so that they learned to like the light box. The research team used this task to deliver GluA1 to synapses in the hippocampus of rats in an earlier study.

　　"Using green light to stimulate the hippocampus of mice, we found that compared with the control group, the mice returned to the dark box faster." The first author of the research group Kato Takemoto pointed out. "This shows that by inactivating GluA1 in the synapses, the fear memory of the mice has been cleared.

　　The specificity of GluA1 receptor action varies with the duration of CALI action after the mouse experiences a fear learning task for the first time. The administration of CALI for up to 2 hours after the first task will lead to bioelectrical activity which allows GluA1 receptors to be delivered to the synapses. However, this bioelectric activity cannot be detected 24 hours after the completion of the first mission. Researchers believe this is evidence that GluA receptors have been replaced by other receptors containing GluA2-related proteins, and this is in line with the fact that mice will not lose their fear memory within 24 hours of being given CALI.