LRRC37B is a human modifier of voltage-gated sodium channels and axon excitability in cortical neurons. (https://pubmed.ncbi.nlm.nih.gov/38134874/)

These scientists did a study to understand why humans are so smart. They found a special gene called LRRC37B that is only found in humans. This gene is responsible for making a receptor in our brain cells called cortical pyramidal neurons (CPNs). These CPNs are important for sending electrical signals in our brain.

The scientists did an experiment where they put the LRRC37B gene into mouse brain cells to see what would happen. They found that when the LRRC37B gene was added, the mouse brain cells became less excitable. This means that they didn't send as many electrical signals as before.

The scientists also discovered that LRRC37B binds to two other things in the brain - a protein called FGF13A and a sodium channel called SCN1B. These two things help control the excitability of brain cells. LRRC37B helps FGF13A reduce the excitability of the brain cells, especially at a specific part of the cell called the axon initial segment (AIS).

To make sure their findings were true for humans too, the scientists also studied brain cells from real human brains. They found that human brain cells with the LRRC37B gene were less excitable, just like the mouse brain cells.

So, this study shows that the LRRC37B gene is important for making our brain cells less excitable, which is one reason why humans are so smart. It also helps us understand more about how our brains work and could help us find new treatments for brain diseases.

Libe-Philippot B., Lejeune A., Wierda K., Louros N., Erkol E., Vlaeminck I., Beckers S., Gaspariunaite V., Bilheu A., Konstantoulea K., Nyitrai H., De Vleeschouwer M., Vennekens KM., Vidal N., Bird TW., Soto DC., Jaspers T., Dewilde M., Dennis MY., Rousseau F., Comoletti D., Schymkowitz J., Theys T., de Wit J., Vanderhaeghen P. LRRC37B is a human modifier of voltage-gated sodium channels and axon excitability in cortical neurons. Cell. 2023 Dec 21;186(26):5766-5783.e25. doi: 10.1016/j.cell.2023.11.028.