1998 November 20 | Takao K. Hensch, Michela Fagioli, Nobuko Mataga, Michael P. Stryker, Steinunn Baekkeskov, and Shera F. Kash
This study investigates the role of GABAergic inhibition in experience-dependent plasticity in the developing visual cortex of mice. The researchers found that a specific GABA-synthesizing enzyme, GAD65, is crucial for the normal development of visual cortex plasticity. Mice lacking GAD65 showed impaired plasticity, but this defect could be reversed by enhancing GABAergic inhibition with benzodiazepines. The study suggests that intrinsic inhibitory interneurons in the visual cortex detect sensory input imbalances to drive plasticity during development. The results indicate that fast GABAergic transmission is necessary for detecting and responding to competitive input from the two eyes. The study also shows that plasticity in GAD65 knockout mice can be restored by enhancing GABAergic inhibition, highlighting the importance of intrinsic inhibitory circuits in visual cortex plasticity. The findings suggest that the balance between excitation and inhibition is critical for normal visual development and that GABAergic transmission is essential for experience-dependent plasticity in the visual cortex. The study provides a model to understand the unique local circuit properties that drive experience-dependent plasticity in the visual cortex.This study investigates the role of GABAergic inhibition in experience-dependent plasticity in the developing visual cortex of mice. The researchers found that a specific GABA-synthesizing enzyme, GAD65, is crucial for the normal development of visual cortex plasticity. Mice lacking GAD65 showed impaired plasticity, but this defect could be reversed by enhancing GABAergic inhibition with benzodiazepines. The study suggests that intrinsic inhibitory interneurons in the visual cortex detect sensory input imbalances to drive plasticity during development. The results indicate that fast GABAergic transmission is necessary for detecting and responding to competitive input from the two eyes. The study also shows that plasticity in GAD65 knockout mice can be restored by enhancing GABAergic inhibition, highlighting the importance of intrinsic inhibitory circuits in visual cortex plasticity. The findings suggest that the balance between excitation and inhibition is critical for normal visual development and that GABAergic transmission is essential for experience-dependent plasticity in the visual cortex. The study provides a model to understand the unique local circuit properties that drive experience-dependent plasticity in the visual cortex.