小鼠实验 z-bo 2020-11-05 344

　　Researchers have shown in mice that it is possible to return adult neural circuits to a younger, immature state by targeting a receptor in the brain called PirB.

　　The development of a therapy that blocks PirB may help patients recover from brain injury or stroke faster, or improve learning and memory in developmental diseases. In critical developmental stages, young brain circuits can be adjusted through rapid learning. They are considered "plastic". Unfortunately, after adulthood, the speed and quality of learning plummeted, and the brain became stubbornly resisting changes in its neural circuits. One way to track plasticity is to monitor the ability to coordinate visual input from both eyes-something the human brain learns to do in the first few months of life.

　　By studying the visual function of adult mice with a kind of "lazy eye" disease, Carla Shatz, together with David Bochner and colleagues found that the adult brain has never actually lost its ability to act in a young manner; it only activates the PirB pathway And closed this ability.

　　The author of the article showed in mice that blocking PirB genetically or biochemically allows the mice to quickly adjust to the loss of vision in one eye-as if they were still pups. The fact that blocking PirB can restore this "lazy eye" condition in adult mice is evidence that it can restore the brain's ability to perform at a young age. When PirB is deleted, it relaxes the neuron’s synapses and reduces the stability of brain circuits so that they can more easily buckle, change and create new circuits.

　　But the researchers cautioned that inhibiting PirB may have negative effects. It may cause instability. Since the human brain has the equivalent of 5 PirB molecules (the mouse only has 1 PirB molecule), it is still unknown whether targeting some or all of the PirBs will help restore brain plasticity in humans.