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During the final weeks of pregnancy, the cerebellum grows larger and develops a complex pattern of folds. The cerebellum is important for movement, language and social interactions. This is likely caused by injuries to a part of the brain called the cerebellum.
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Preterm infants have a higher risk of developing movement difficulties and neurodevelopmental conditions like autism spectrum disorder. These data argue that excitatory cerebellar neurons define the maturation time-window for postnatal Purkinje cell functions and refine cerebellar-dependent behaviors. We also show that our mutant pups have impaired motor behaviors and vocal skills. We reveal that Purkinje cells fail to acquire their typical morphology and connectivity, and that the concomitant transformation of Purkinje cell firing activity does not occur either. We generated mutant mice that lack the majority of excitatory cerebellar neurons and tracked the structural and functional consequences on Purkinje cells. Here, we use regional genetic manipulations and in vivo electrophysiology to test whether excitatory neurons establish the firing properties of Purkinje cells during postnatal mouse development. Excitatory granule cells, the most numerous neuron type in the brain, are especially vulnerable and likely instigate disease by impairing the function of their targets, the Purkinje cells. Preterm infants that suffer cerebellar insults often develop motor disorders and cognitive difficulty.