Researchers found in mice that targeting a receptor called PirB in the brain can restore adult neural circuits to a young, immature state. The development of treatments that block PirB can help patients recover from brain injuries and strokes faster, and can improve learning and memory development disorders. At the critical stage of development, young brain circuits can be adjusted through rapid learning. They are considered "plastic". Unfortunately, in adulthood, the speed and quality of learning plummet, and the brain becomes tenaciously resistant to changes in neural circuits. One way to track plasticity is to monitor the ability to coordinate binocular visual input. It learns what the human brain has learned in the first few months of life. By studying the visual function of adult mice with "lazy eye" disease, Carrashats, David Bockner and colleagues together lost the ability of the adult brain to actually play a young role. It was found that it only activated the PirB pathway and turned off this feature.
The author of the article showed that blocking PirB in mice through genetic or biochemical methods can quickly adapt to the loss of vision in one eye. PirB blockers can restore this "lazy eye" state in adult mice, and this fact proves that it can restore the brain's ability to perform at an early age. After removing PirB, neuron synapses will relax and the stability of brain circuits will be reduced, making it easier to bend, modify and create new circuits.
But the researchers warned that blocking PirB may have adverse consequences. It may become unstable. Since the human brain is equivalent to five PirB molecules (the mouse has only one PirB molecule), it is not clear whether targeting some or all of PirB can restore the plasticity of the human brain.