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Here, we used functional, morphological, and viral-mediated approaches to uncover the pathogenic contribution of unbalanced excitation-inhibition in a mouse model of spinal muscular atrophy (SMA). We show that vulnerable SMA motor circuits fail to respond homeostatically to reduced excitation and instead increase inhibition. This imposes an excessive burden on motor neurons and further restricts their recruitment. Reducing inhibition genetically or pharmacologically improves neuronal function and motor behavior in SMA mice. 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