Nf1 is required during early, but not late, cerebellar development to facilitate neuronal lamination, providing a potential therapeutic prevention strategy for NF1-associated developmental abnormalities.
Different Purkinje cell subpopulations show distinct developmental profiles of physiological activity, climbing fiber inputs and axonal and dendritic morphology, matching different timelines of cerebellum-dependent behaviors.
Building on previous work (Haldipur et al., 2014), we show that many key mechanisms controlling cerebellar development are likely conserved between mouse and human, and validate our mouse model of Dandy-Walker malformation.
Electrophysiological analysis and imaging in live zebrafish reveal that infant- and adult-onset SCA13 mutations have distinct effects on the electrical activity, development, and survival of cerebellar Purkinje cells.
The first born excitatory cerebellar nuclei neurons influence the survival of their Purkinje cell partners which stimulate the expansion of granule cells and interneurons to produce functional local circuits.